Dermatoveneorology PDF

DCM 3106: DERMATO-VENEREOLOGY I
WEEK CONTENT
WEEK 1 Anatomy and physiology of skin.
WEEK 2 History taking and physical examination in dermatology

General principles of diagnosis and management of skin conditions.
WEEK 3 Infectious skin conditions
Disturbances in pigmentation
WEEK 4 Blistering diseases
Drug reactions
Cutaneous manifestations of systemic diseases
WEEK 5 CAT 1
WEEK 6 Icthyosis
Eczema
Psoriasis
Erythroderma
WEEK 7 Bacterial STIs
Parasitic STIs
WEEK 8 Viral STIs
WEEK 9 Fungal STIs
WEEK 10 CAT 2
WEEK 11 MAIN EXAM
WEEK 12 MAIN EXAM
CORE READING MATERIALS

McCree D. H, Jones K.T, O’Leary A. (2008). African Americans and HIV/AIDS. Springer-Verlag New York Inc.978-
0-387-78320-8 (ISBN).
Rebat M. Taylor & Francis. (2006). Dermatology and Dermatological Therapy of Pigmented Skins.
ANATOMY AND PHYSIOLOGY OF SKIN
THE CUTANEOUS MEMBRANE

The cutaneous membrane is the technical term for our skin. The skin’s primary role is to help protect the rest of the body’s
tissues and organs from physical damage such as abrasions, chemical damage such as detergents, and biological damage
from microorganisms. For example, while the skin harbors many permanent and transient bacteria, these bacteria are unable
to enter the body when healthy, intact skin is present.
Our skin is made of three general layers. In order from most superficial to deepest they are the epidermis, dermis, and
subcutaneous tissue.
THE EPIDERMIS
The epidermis is a thin layer of skin. It is the most superficial layer of skin, the layer you see with your eyes when you look at
the skin anywhere on your body. Functions of the epidermis include touch sensation and protection against microorganisms.
This skin is further divided into five, separate layers. In order from most superficial to deepest, they are the:
 Stratum Corneum: This layer is composed of the many dead skin cells that you shed into the environment—as a
result, these cells are found in dust throughout your home. This layer helps to repel water.
 Stratum Lucidum: This layer is found only on the palms of the hands, fingertips, and the soles of the feet.
 Stratum Granulosum: This is the layer where part of keratin production occurs. Keratin is a protein that is the main
component of skin.
 Stratum Spinosum: This layer gives the skin strength as well as flexibility.
 Stratum Basale: This is where the skin’s most important cells, called keratinocytes, are formed before moving up to
the surface of the epidermis and being shed into the environment as dead skin cells.
This layer also contains melanocytes, the cells that are largely responsible for determining the color of our skin and protecting
our skin from the harmful effects of UV radiation. These harmful effects include burns in the short term and cancer in the
long run.
THE DERMIS
Underneath the epidermis lies the dermis. The dermis contains:
 Blood vessels that nourish the skin with oxygen and nutrients. The blood vessels also allow immune system cells to
come to the skin to fight an infection. These vessels also help carry away waste products.
 Nerves that help us relay signals coming from the skin. These signals include touch, temperature, pressure, pain, and
itching.
 Various glands.
 Hair follicles.
 Collagen, a protein that is responsible for giving skin strength and a bit of elasticity.
Dermal layers
Papillary dermis
| Medicine VI: Mental health and dermato-veneorology 2

The papillary dermis is the uppermost layer of the dermis. It intertwines with the rete ridges of the epidermis and is composed
of fine and loosely arranged collagen fibers. The papillary region is composed of loose areolar connective tissue. This is
named for its fingerlike projections called papillae, that extend toward the epidermis and contain either terminal networks of
blood capillaries or tactile Meissner's corpuscles.
Reticular dermis
The reticular dermis is the lower layer of the dermis, found under the papillary dermis, composed of dense irregular connective
tissue featuring densely packed collagen fibers. It is the primary location of dermal elastic fibers.
The reticular region is usually much thicker than the overlying papillary dermis. It receives its name from the dense
concentration of collagenous, elastic, and reticular fibers that weave throughout it. These protein fibers give the dermis its
properties of strength, extensibility, and elasticity. Within the reticular region are the roots of the hair, sebaceous glands,
sweat glands, receptors, nails, and blood vessels. The orientation of collagen fibers within the reticular dermis creates lines of
tension called Langer's lines, which are of some relevance in surgery and wound healing.
THE HYPODERMIS

Beneath the dermis is the deepest layer of our skin. It is alternatively termed hypodermis, subcutis, or subcutaneous tissue. It
contains many collagen cells as well as fat.
Fat, in particular, helps insulate our body from the cold and act as a cushion for our internal structures (such as muscles and
organs) when something hits us. Fat can also be called upon by the body in times of great need as an energy source.
Given the alternative names for this layer, it should come as no surprise that this is the layer where subcutaneous injections
are given into via a hypodermic needle.
THE SUBCUTANEOUS TISSUE

The deepest layer of the skin is called the subcutaneous layer, the subcutis, or the hypodermis. Like the dermis, the layer
contains blood vessels and nerves for much the same reasons.
Importantly, the subcutis contains a layer of fat. This layer of fat works alongside the blood vessels to maintain an appropriate
body temperature. The layer of fat here acts as a cushion against physical trauma to internal organs, muscles, and bones.
Additionally, the body will turn to this fat in times of starvation to provide power to its various processes, especially brain
function.
FUNCTIONS OF THE SKIN

The skin is an organ of protection. The primary function of the skin is to act as a barrier. The skin provides protection from:
mechanical impacts and pressure, variations in temperature, micro-organisms, radiation and chemicals.
The skin is an organ of regulation. The skin regulates several aspects of physiology, including: body temperature via sweat
and hair, and changes in peripheral circulation and fluid balance via sweat. It also acts as a reservoir for the synthesis of
Vitamin D.
The skin is an organ of sensation. The skin contains an extensive network of nerve cells that detect and relay changes in the
environment. There are separate receptors for heat, cold, touch, and pain. Damage to these nerve cells is known as
neuropathy, which results in a loss of sensation in the affected areas. Patients with neuropathy may not feel pain when they
suffer injury, increasing the risk of severe wounding or the worsening of an existing wound.
The skin has very important vital functions for keeping the physiological and biochemical conditions of the body in its
optimum state. The most important functions of the skin are:
1. Regulates body temperature.
2. Prevents loss of essential body fluids, and penetration of toxic substances.
3. Protection of the body from harmful effects of the sun and radiation.
4. Excretes toxic substances with sweat.
5. Mechanical support.
6. Immunological function mediated by Langerhans cells.
7. Sensory organ for touch, heat, cold, socio-sexual and emotional sensations.
8. Vitamin D synthesis from its precursors under the effect of sunlight and introversion of steroids.
FACTORS AFFECTING SKIN PENETRATION

The penetration of substances through the skin surface depends upon different factors:
a) Age - penetration is more in newborn and children than in adults.
b) Skin condition - penetration is more on injured or abraded skin surfaces. Chemicals may cause injury and increase
penetration.
c) Hydration of the skin - penetration is more in hydrated skin than dry skin. Hydration increases the permeability of the
stratum corneum. Water is an effective penetration enhancer.
d) Fat content of the epidermis has no much effect on penetration.
e) Type of vehicles: vehicles may increase penetration and absorption of the drug from the skin surface. This depends on
the type of vehicle and the condition of the skin. Certain vehicles that may cause injury to the skin even minimal injury
predispose to more penetration of the drugs or other materials applied topically to the skin surface.
f) Hyperemia - vasodilatation of the blood vessels in response to different stimuli either local or generalized increases the
penetration.
g) Physiological and pharmacological factors
h) The penetration in vivo of topically applied substances can be assessed by physiological or pharmacological signs or
analyzed by chemical or histological techniques:
 Vasoconstriction has been utilized for corticosteroids.
 Vasodilatation for nicotinates.
 Whealing for histamines.
 Sweating for pilocarpine.
 Anesthesia for local anesthetics.
i) Lipoid soluble substances facilitate penetration of substances applied to the skin surface. Steroid hormones and vitamin
D, salts such as chloride and sulfate can penetrate the skin surface. Gases and volatile substances can pass through the
skin.

2. HISTORY TAKING AND PHYSICAL EXAMINATION
IN DERMATOLOGY
HISTORY TAKING
SOCRATES
 Site: covered vs. sun exposed.
 Site: symmetrical vs. asymmetrical.
 Site: where originated, if spread, when it moved.
 Site: arrangement pattern.
 Character: colour, shape, depression/elevation, edges.
 Character: changes in properties.
 Character: itchiness, pain.
 Character: scaling, crusting.
 Character: discharge, bleeding.
PAST MEDICAL, SURGICAL HISTORY

Similar condition in the past.
 DM (lower limb ulcerations).
 Asthma, hayfever (eczema).
 Strep (erythema nodosum).
 Rash dz's: psoriasis, RA, herpes, etc.
 Family history
 Similar condition in a relative, what age.
 Skin problems in the family.
 Allergies in the family.
SOCIAL HISTORY
Smoking: ever smoked, how many per day, for how long, type [cigarette, pipe, chew].
Passive smoking in the home, workplace.
Alcohol (aspiration).
Occupation type.
Occupation details:
• Tasks done at work.
• Chemicals, plants contacted.
• How long of exposure.
• Protection used.

• Illness in fellow workers.
Pets at home (allergy).
Stress levels (allopecia, etc).
Who is with you there at home.
Drug history
Drugs currently, formerly on:
• Steroids (thinning, bruising, ulceration).
• Chemotherapy (allopecia).
• Dyes (hives).
OTCs:
• Salves.
• Shampoos.
Ventilators.
Recreational drugs:
• IV drugs.
Allergies:
• Chemicals.
• Latex.
Allergies to drugs, esp. rashes:
• Drugs.
• Dyes.
PHYSICAL EXAMINATION
a) Environment
N/A so far.
b) General appearance
Pt undresses, so entire skin can be examined.
Pt. is scratching.
c) Inspect: entire skin

 Dry skin (hypothyroid).
 Thick skin (acromegaly, androgens).
 Thin skin (Cushing's, hypothyroid, liver dz).
 Stretched skin (scleroderma).
 Scratch marks.
 Swollen lymph nodes.
 Systemic rash.
Inspect: lesion

Location:
• Sun exposed vs. covered.
• Asymmetrical vs. symmetrical.
• Number.
• Peripheral vs. trunk.
• Hallmark locations. See Hallmark Rashes Reference.
Pattern:
• See Skin Lesion Patterns Reference.
• Discrete vs. confluent.
Colour.
Size.
Shape.
Edges:
• Well demarcated vs. poorly demarcated.
Surface:
• Scaling, crusting.
• Shiny vs. dull.
• Thickening, blistering.
• Ulceration, skin breaks, fissures.
• Elevation.
Discharge, bleeding.
Type of lesion. See Skin Lesion Terminology Reference.
d) Palpate: lesions
Ask pt. if tender, first.
Palpate lesions/masses. See Examining A Mass Reference.
Flat vs. raised.
Temperature (inflammatory).
Apply pressure:
• Blanches on pressure.
• Doesn't blanche on pressure (purpura).
If inflammation or carcinoma: palpate draining nodes for the lesions.
SKIN LESIONS
DISTRIBUTION
Distribution refers to how the skin lesions are scattered or spread out. Skin lesions may be isolated (solitary or single) or
multiple. The localisation of multiple lesions in certain regions helps diagnosis, as skin diseases tend to have characteristic
distributions. What is the extent of the eruption and its pattern?
a) Acral – affects distal portions of limbs (hand, foot) and head (ears, nose).
b) Blaschko lines – following a roughly linear, segmental pattern described by Blaschko and thought to be indicative of
somatic mosaicism.
c) Dermatomal – corresponding with nerve root distribution.
d) Extensor – involving extensor surfaces of limbs. Contrast with flexor surfaces.
e) Flexural – involving skin flexures (body folds); also known as intertriginous.
f) Follicular – individual lesions arise from hair follicles. These may be grouped into confluent plaques.
g) Generalised – universal distribution: may be mild or severe, scattered or diffuse
h) Herpetiform – grouped umbilicated vesicles, as arise in Herpes simplex and Herpes zoster infections.
i) Koebnerised – arising in a wound or scar. The Koebner phenomenon refers to the tendency of several skin conditions to
affect areas subjected to injury.
j) Photosensitive – favouring sun exposed areas. Does not affect skin that is always covered by clothing.
k) Head and neck: spares eyelids, depth of wrinkles and furrows, areas shadowed by hair, nose and chin. Typically involves
“V” of neck.
l) Backs of hands: spares finger webs. More severe on proximal than distal phalanges.
m) Forearms: extensor rather than flexor.
n) Feet: dorsal surface, sparing areas covered by footwear.
o) Lower legs: may affect extensor and/or flexor surfaces
p) Trunk: rarely affected
q) Pressure areas– affecting areas regularly prone to injury from pressure at rest.
 Tops of the ears when sleeping
 Buttocks when sitting
 Heels when lying
r) Seborrhoeic – the areas generally affected by seborrhoeic dermatitis, with a tendency to oily skin (seborrhoea). Scalp,
behind ears, eyebrows, nasolabial folds, sternum and interscapular.
s) Symmetrical – in the same regions, the left side is affected in a similar way to the right side.
t) Truncal – favours trunk and rarely affects limbs.
u) Unilateral – wholly or predominantly on one side of the affected region.
CONFIGURATION OF LESIONS
Configuration refers to the shape or outline of the skin lesions. Skin lesions are often grouped together. The pattern or shape
may help in diagnosis as many skin conditions have characteristic configuration.
 Nummular lesion – round (coin-shaped) lesions. Also known as discoid.
 Linear lesion – a linear shape to a lesion often occurs for some external reason such as scratching. Also striate.
 Target lesion – concentric rings like a dartboard. Also known as iris lesion.
 Gyrate rash – a rash that appears to be whirling in a circle.

 Annular – lesions grouped in a circle.
COLOUR
Descriptive terms used to describe skin colour include:
 Carotenaemia – excessive circulating beta-carotene (vitamin a precursor derived from yellow/orange coloured vegetables
and fruit) results in yellow/orange skin colouration. Tends to be pronounced on palms and soles. Does not affect cornea.
 Hyperpigmentation – hypermelanosis or haemosiderin deposits result in skin colour that is darker than normal.
 Hypopigmentation – loss of melanin results in skin colour that is paler than normal but not completely white.
 Leukoderma – white skin. Also known as achromia.
 Infarcts – black areas of necrotic tissue due to interrupted blood supply.
 Jaundice – excessive circulating bilirubin results in yellow/green skin colour, prominent in cornea.
 Erythema – red skin due to increased blood supply and blanch with pressure (“diascopy”).
 Erythroderma – the skin condition affects the whole body or nearly the whole body, which is red all over.
 Telangiectasia – prominent cutaneous blood vessels.
 Purpura – bleeding into the skin. This may be as petechiae (small red, purple or brown spots) or ecchymoses (bruises).
Purpura does not blanch with pressure (diascopy).
MORPHOLOGY
Morphology is the form or structure of an individual skin lesion.
a) Skin lesions may be flat, elevated above the plane of the skin or depressed below the plane of the skin.
b) They may be skin coloured or red, pink, violaceous, brown, black, grey, blue, orange, yellow.
c) Consistency may be soft, firm, hard, fluctuant or sclerosed (scarred or board-like).
d) The lesions may be hotter or cooler than surrounding skin.
e) They may be mobile or immobile.
f) Macule – an area of colour change less than 1.5 cm diameter. The surface is smooth.
g) Patch – a large area of colour change, with smooth surface.
h) Papule – a small palpable lesion. The usual definition is that they are less than 0.5 cm diameter, although some authors
allow up to 1.5 cm. They are raised above the skin surface, and may be solitary or multiple. Papules may be:
 Acuminate (pointed)
 Dome-shaped (rounded)
 Filiform (thread-like)
 Flat-topped
 Oval or round
 Pedunculated (with a stalk)
 Sessile (without a stalk)
 Umbilicated (with a central depression)
 Verrucous (warty)
i) Nodule – an enlargement of a papule in three dimensions (height, width, length). It is a solid lesion.
j) Cyst – a papule or nodule that contains fluid, so is fluctuant.

k) A plaque is a palpable flat lesion usually greater than 1 cm diameter. Most plaques are elevated, but a plaque can also
be a thickened area without being visibly raised above the skin surface. They may have well-defined or ill-defined borders.
The name 'plaque' is derived from the French word for plate. Plaques may be:
 Annular (ring shaped)
 Arcuate (half-moon)
 Polygonal (varied non-geometric shape)
 Polymorphic (varied shape)
 Serpiginous (in the shape of a snake)
 Poikilodermatous (variegated appearance, usually mixed pallor, telangiectasia and pigmentation)
l) Vesicle – small fluid-filled blister less than 0.5cm diameter. They may be single or multiple.
m) Pustule – a purulent vesicle. It is filled with neutrophils, and may be white, or yellow. Not all pustules are infected.
n) Bulla – a large fluid-filled blister. It may be a single compartment or multiloculated.
o) Abscess is a localised collection of pus.
p) Weal – an oedematous papule or plaque caused by swelling in the dermis. Wealing often indicates urticaria.
SKIN SURFACE
The skin surface of a skin lesion may be normal or smooth because the pathological process is below the surface, either
dermal or subcutaneous. Surface changes indicate epidermal changes are present.
Scaling or hyperkeratosis – an increase in the dead cells on the surface of the skin (stratum corneum). Descriptive terms for
scale include:
 Desquamation (skin coming off in scales)
 Psoriasiform (large white or silver flakes)
 Pityriasiform (branny powdery scale)
 Lichenoid (apparent scale is tightly adherent to skin surface)
 Keratotic (horny scale)
 Exfoliation (peeling skin)
 Maceration (moist peeling skin)
 Verrucous (warty)
SECONDARY CHANGES
 Lichenification – caused by chronic rubbing, which results in palpably thickened skin with increased skin markings and
lichenoid scale. It occurs in chronic atopic eczema and lichen simplex.
 Crusting – the result of plasma exuding through an eroded epidermis. It is rough on the surface and is yellow or brown
in colour. Bloody crust appears red, purple or black.
 Dystrophy – degeneration or abnormal formation of the skin. It is often used to refer to nail diseases.
 Excoriation – a scratch mark. It may be linear or a picked scratch (prurigo). Excoriations may occur in the absence of a
primary dermatosis.
 Erosion – caused by loss of the surface of a skin lesion; it is a shallow moist or crusted lesion.
 Fissure – a thin crack within epidermis or epithelium, and is due to excessive dryness.

 Fungating – refers to a large malignant tumour that is erupting like a mushroom or fungus.
 Granulation tissue – made of a mass of new capillaries and fibrous tissue in a healing wound.
 Ulcer – full thickness loss of epidermis or epithelium. It may be covered with a dark-coloured crust called an eschar.
 Granuloma – a histological (pathological) term refering to chronic inflammation in which there are several types of
inflammatory cells including giant cells. Granulomas form in response to foreign bodies, certain infections (tuberculosis,
leprosy) and inflammatory skin diseases (granuloma annulare, granuloma faciale, sarcoidosis).
 Hypertrophy – some component of the skin such as a scar is enlarged or has grown excessively. The opposite is atrophy
or thinned skin.

2. GENERAL PRINCIPLES OF DIAGNOSIS AND
MANAGEMENT OF SKIN CONDITIONS
GENERAL MANAGEMENT
In skin conditions generally and particularly in the acute varieties rest may be an essential feature of treatment. The skin is an
organ of complex physiology, and in any form of inflammation its functions must be upset. Complete rest in bed will place
this organ, the largest by far in the body, under conditions where it can continue work with the minimum amount of friction
and tension.
While physical rest is of great importance, mental rest must be enjoined as far as possible. In acute and generalized skin
conditions, rest from worry and anxiety is of the utmost importance and sufficient rest must be assured by sedatives and
hypnotics if necessary.
Nursing should be both sympathetic and skilled, in order that local remedies should be properly applied, and to counteract
the depression often found with chronic and generalized skin conditions. Removal from overcrowded and unhealthy
surroundings facilitates recovery from skin affections, and it is sometimes amazing to see the acceleration in healing when
patients who have been treating themselves at home are admitted to hospital or nursing home. Ideally, a period of
convalescence before returning to the daily routine is of value after treatment, both from the point of view of change of air,
and of healthy exercise and freedom from worry. Patients who have had acute skin conditions on the exposed parts of the
body should not be exposed to sun and wind, but chronic skin conditions on other parts of the body often do well at the
seaside.
Differences of opinion are frequent over the question of diet. Patients who are acutely ill and suffering from fever should be
treated with the usual fluid diet, but as a general rule, a bland and nutritious diet does no harm. Anything which increases
flushing is harmful, and in this connection alcohol, strong tea and coffee and condiments are best completely avoided.
Indigestible foods such as cheese, nuts, shellfish and pastry should be taken in the strictest moderation or not at all. Certain
diseases do seem to benefit by special dietary measures.
Sufferers from acne or seborrhoea do better on a low fat diet, especially avoiding chocolate and cocoa. Psoriasis has also
been claimed (Griitz and Burger) to be favourably affected by a low fat diet. Rosacea usually responds well to diet, and here
hot drinks (especially tea and coffee) and alcohol should be eschewed.
In my experience, infantile eczema is not usually caused by food allergens, and therefore does not usually benefit by diet, but
occasionally cases are met where the withdrawal of some food like egg, milk, wheat or barley assists in recovery. Tuberculosis
of the skin has been favourably influenced by a salt free diet, but requires other treatment as well.
LOCAL TREATMENT
At the present time local treatment properly applied, is still our most potent weapon in the management of skin diseases,
although environmental change and internal medication are assuming a much greater importance than they did in the past.
It is important, of course, to make a diagnosis as soon as possible, and, in some diseases, essential to do so, but for this
pathological freedom from worry. Patients who have had acute skin conditions on the exposed parts of the body should not
be exposed to sun and wind, but chronic skin conditions on other parts of the body often do well at the seaside.
Differences of opinion are frequent over the question of diet. Patients who are acutely ill and suffering from fever should be
treated with the usual fluid diet, but as a general rule, a bland and nutritious diet does no harm. Anything which increases
flushing is harmful, and in this connection alcohol, strong tea and coffee and condiments are best completely avoided.
Indigestible foods such as cheese, nuts, shellfish and pastry should be taken in the strictest moderation or not at all. Certain
diseases do seem to benefit by special dietary measures.
Sufferers from acne or seborrhoea do better on a low fat diet, especially avoiding chocolate and cocoa. Psoriasis has also
been claimed (Griitz and Burger) to be favorably affected by a low fat diet. Rosacea usually responds well to diet, and here
hot drinks (especially tea and coffee) and alcohol should be eschewed.
Infantile eczema is not usually caused by food allergens, and therefore does not usually benefit by diet, but occasionally cases
are met where the withdrawal of some food like egg, milk, wheat or barley assists in recovery. Tuberculosis of the skin has
been favorably influenced by a salt free diet, but requires other treatment as well.
LOCAL TREATMENT
At the present time local treatment properly applied, is still our most potent weapon in the management of skin diseases,
although environmental change and internal medication are assuming a much greater importance than they did in the past.
It is important, of course, to make a diagnosis as soon as possible, and, in some diseases, essential to do so, but for this
pathological investigations or expert opinion may be required, and it becomes necessary to treat the patient while these
investigations are being undertaken, or until expert opinion is obtained. Many cutaneous conditions may be alleviated by
rational local treatment, especially if certain aspects of the diseases are borne in mind, and one should look for them in the
following order. First the phase of activity, acute, subacute, or chronic should be judged, followed by the type and
characteristics of the eruption and finally the location.
Treatment can be started immediately if these principles are followed, and I hope to show simply how this can be done. I
have divided skin diseases into the following five empirical groups:
(a) Crusted conditions,
(b) Infected conditions,
(c) Acute conditions,
(d) Subacute conditions,
(e) Chronic conditions.
Before proceeding further, I would stress that strong local medicaments should never be used, unless one is certain of the
diagnosis of the condition, and is using the medicament in a specific manner. I should like to utter a word of warning about
the local treatment of sulphonamides on the skin. One still meets too many cases of sensitization induced by local treatment
with sulphonamides, and this sensitivity may last for a long time. Where these drugs are indicated, it is my practice to use full
doses of sulphonamides internally; and the results are very satisfactory.

Any of the acute, subacute or chronic conditions may be, and often are, infected or crusted or both, and this must be dealt
with first, but I haye put crusting and infection in separate categories in order better to establish some general principles of
treatment.
A. CRUSTED CONDITIONS
Crusts harbour infection and secretions, and further prevent medicaments from coming into contact with the affected parts.
Where present over large areas of the body, or in the flexures, crusts may best be removed by baths, but in smaller areas or
on the scalp, may be removed by borostarch poultices or the application of oil.
Simple baths of warm water and curd soap may be used for cleansing purposes, but often where the skin is inflamed and
irritable, soap and water will not be tolerated. Here I prefer an emollient bath which will loosen crusts, and relieve itching and
inflammation. This is made by adding i or 2 lbs. of bran or oatmeal to the bath in the following manner. The bran or oatmeal
is tied up in a gauze or muslin bag under the hot water tap which is allowed to run through the contents. The bag is then
removed and placed in the bath, while cold water is added until a suitable temperature is reached.
Smaller areas may be treated with oil packs of olive or arachis oil, or borostarch poultices may be applied. These are made
by adding one teaspoonful of boric acid to four tablespoonfuls of starch, making into a paste with a little cold water, and
pouring on a pint of boiling water. When cold, this poultice is spread thickly on muslin and applied frequently, renewing the
poultice every hour until the desired effect is obtained.
B. INFECTED CONDITIONS
This is a common complication of almost any form of skin disease, and usually must be dealt with first, or possibly in
combination with early treatment. Strong antiseptics should be avoided, as they tend to increase inflammation of the skin.
Where a large area of the body is affected, potassium permanganate baths are useful, made by adding 2 drachms of the
drug to a 30 gallon bath.
The permanganate of potassium should be in solution before being added to the bath in order to avoid severe staining, and
the patient could have a daily bath of about 20 minutes.
Limbs can be treated in the same way with 1:10000 permanganate baths three times daily for 20 minutes, and usually respond
well.
Milder conditions could be treated by adding a mild antiseptic to the medicament being used. For example, 1- or 1% Gentian
violet, or 1% brilliant green are easily incorporated with lotions, liniments, creams or pastes.
Penicillin spray or cream (for acute skin conditions the spray rather than the cream) at a strength of 10,000 units per c.c. or
gram can be used as a preliminary measure to clean up superficial infection, or for deeper infection, such as boils, erysipelas
or cellulitis, full doses of sulphonamides by mouth or penicillin by injection are valuable. These should be discontinued as
soon as infection is suppressed and ordinary treatment continued.

C. ACUTE CONDITIONS
These should always be treated with soothing, wet dressings and bland lotions until the condition subsides. The acute form
may be erythematous, vesicular or oozing, and in extremely acute cases may not tolerate even the most simple medicaments.
Here frequent normal saline compresses may be used, or a 2-3 per cent. solution of boric acid. But usually the skin, even if
weeping freely, tolerates lead lotion which acts as a cooling, astringent and anti-pruritic lotion. Lead lotion can be freshly
prepared as required by adding one drachm of liquor plumbi subacetate fort. (B.P.) to a pint of cokl tap water. White lint to
size required is cut and dipped into the lotion, until it is sopping, but not running, and then applied to the affected part.
The dressing may be re-dipped and re-applied as often as necessary, but always before it dries. It is my practice not to cover
the lint at all, or at most by a turn or two of open-wove bandage, in order to obtain the maximum cooling effect. Applied in
this way, an oozing surface will dry well often in only a day or two, when calamine lotion or liniment may be substituted.
Large areas, especially in elderly people, should not be treated-in this manner because of the marked chilling effect. At night
the treatment should be interrupted to allow the patient to sleep and then calamine lotion may be used.
Where there is simple erythema, lotion calaminae B.P.C., may be the first dressing, and as the part dries, a liniment or cream
may be substituted as for the subacute phase.
D. SUBACUTE CONDITIONS
This may arise de novo, or be seen following the acute condition when oozing or erythema is subsiding and the part is
becoming scaly. Simple liniments or creams may be used to advantage, and I prefer the cremor zincii B.P.C., or the following
calamine liniment:
Calamine prep. ................... gr. 30
Zinc oxide ....................... gr. 30
Liquor caliis ...................... 3 2
01. Olivae (or 01. Arachis)
To both of these preparations, medicaments may be added if necessary. Thus in conditions of general inflammation and in
seborrhoeic dermatitis i or 2 per cent. ichthyol is very useful, or i per cent. sulphur in seborrhoeic conditions too. Antiseptics
like gentian violet 1% or brilliant green 1%. can be added without harm for mildly infected conditions. Carbolic acid has a
marked antipruritic action, as well as antiseptic and anesthetic, and is useful in 1% strength or, at the most ½%. The liniment
is less drying than the cream, which might be reserved for the final stages of this phase. Very often no further treatment is
needed, as the condition will subside completely.
I prefer these medicaments to be applied with a soft 1 inch paint brush as the spread is easier and more even, and it is simpler
for nurse or patient to use. (I advise this too with calamine lotion in the acute phase.) The part should be kept exposed to air
as much as possible, and left uncovered or covered with a single layer of gauze. Bedclothes may be kept off the body by
means of a cradle, and this adds to the comfort of the patient and assists healing.
E. CHRONIC CONIDITIONS
Here there is usually no emergency and every effort should be made to reach a diagnosis before beginning treatment, since
specific remedies are added to the various medicaments.

In eczematous types of eruptions, chronic conditions may follow the subacute, and it may be necessary to treat chronic scaly
and lichenified areas.
Ointments and pastes are of great use here.
Pastes differ from ointments in having a larger proportion of powder in the greasy base, and so absorbing discharges and
exudates better.
For example, zinc paste,
Starch ............................ 3 2
Zinc oxide ......................... 3 2
Lanolin ............................ . 2
Vaseline ........................... 3 2
which contains 50% powder and 50% greasy base, whereas a zinc ointment would be
Zinc oxide ........................ 3 2
Lanolin ......................... 3 2
Vaseline ........................ . 3 4
Pastes are thicker, drier and more absorbent than ointments and penetrate less deeply, and incorporated ingredients are less
active in pastes, which may be used on lesions with a tendency to crusting or vesiculation.
An ointment under these conditions would be more heating and macerating and therefore less suitable.
Acute dermatoses reaching the chronic state are often completely healed by the final application of the above bland paste,
to which 2% of salicylic acid may be usefully added (Lassar's paste). Where more penetration is required in the active treatment
of specific dermatoses, medicaments may be incorporated into ointment bases, and'
Sulphur ppt. . .. ................. .gr. io
Salicylic acid ...................... gr. io
Lanolin ........................ 3 2
Vaseline ....................... ad
(Lanolin may be difficult to obtain now and may be omitted.) is a useful prescription in chronic seborrhoeic dermatitis. In
psoriasis an ointment is preferable, such as
Salicylic acid ...................... gr. o
Hydrog. ammon. ................ gr. o1
Liq. picis carb. ................... m. 30
Vaseline ........................ ad 5 i
And the amount of salicylic acid may be increased if there is much scaling.
For the scalp one of the newer penetrating bases is preferred as vaseline tends to stick on top of the hair and unguentum
H.E.B. simplex (Halden) may be used instead of the
vaseline and this is more easily washed off.
For the chronic lichenified eruptions, the incorporation of tar as crude coal tar 2% in zinc ointment has an antipruritic and
reducing action, but tar does not suit every case and should be employed with care.

3. INFECTIOUS SKIN CONDITIONS
BACTERIAL SKIN CONDITIONS

Bacterial skin infections can be classified as skin and soft tissue infections (SSTI) and acute bacterial skin and skin structure
infections (ABSSSI). SSTI include
 Impetigo
 Minor cutaneous abscesses
ABSSSI are complex bacterial skin infections. They include

 Cellulitis
 Erysipelas
 Wound infections
 Major cutaneous abscesses (>75 cm2 edema, erythema, and induration)
The primary pathogens in SSTI are Streptococcus and Staphylococcus species, including methicillin-resistant Staphylococcus
aureus (MRSA). MRSA is the most common pathogen in the US. More than half of community-associated SSTI treated in the
US were attributable to MRSA USA300 subtype in the early 2010 decade. However, the proportion of cases attributed to
MRSA differs substantially elsewhere in the world. Particularly because MRSA can be resistant to multiple antibiotics,
recommended antibiotics for bacterial skin and soft tissue infections depend largely on local prevalence and resistance
patterns of MRSA.
The Infectious Diseases Society of America (IDSA) recommends that mild to moderate nonpurulent ABSSSI be treated with a
beta-lactam or clindamycin as presumptive coverage for streptococci. Coverage for MRSA should be considered as well in
patients at risk (eg, after penetrating trauma, with suspected nasal MRSA carriage, or who use IV drugs). Purulent ABSSSI are
considered severe if patients have signs of systemic toxicity (eg, fever, tachycardia, tachypnea, delirium, leukocytosis). If so,
Gram stain, culture, and antibiotic therapy are recommended. The antibiotic of choice is usually vancomycin. However, several
alternatives are available.
MYCOBACTERIAL CONDITIONS
LEPROMATOUS LEPROSY
Lepromatous leprosy is a form of leprosy characterized by pale macules in the skin.
It results from the failure of Th1 cell activation which is necessary to eradicate the mycobacteria (Th1 response is required to
activate macrophages that engulf and contain the disease). In lepromatous leprosy, TH2 response is turned on, and because
of reciprocal inhibition (IL-4; IL-10), the cell-mediated response (TH1) is depressed.

This debilitating form of leprosy begins to spread causing the eyebrows to disappear and spongy tumor like swellings appear
on the face and body. The disease attacks the internal organs, bones, joints and marrow of the body resulting in physical
degeneration. The result is deformity with loss of feeling in the fingers and toes which eventually fall off. Contrary to popular
belief, both forms of leprosy are curable, with the lepromatous form classically treated with antibiotics Dapsone, Rifampin
and Clofazimine for as long as 2–5 years, but if left untreated the person may die up to 20 or 30 years from its inception.
Early detection of the disease is of utmost importance, since severe physical and neurological damage are irreversible even
if cured (e.g. blindness, loss of digits/limbs/sensation). Early infection is characterized by a well demarcated, usually pale, skin
lesion which has lost its hair, and there may be many of these lesions if the infection is more severe (most commonly found
on the cooler parts of the body such as the elbows, knees, fingers, or scrotum, as the bacteria thrive in cooler environments).
This early presentation is the same for both tuberculous and lepromatous forms of leprosy as they are a spectrum of the
same disease (lepromatous being the more contagious and severe form in patients with impaired Th1 response). Disease
progression is extremely slow, and signs of infection may not appear for years.
Family members, and especially children, who have family members with the disease are most at risk. The disease is believed
to be spread through respiratory droplets in close quarters like its relative Mycobacterium tuberculosis, and similarly requires
extended exposure to an individual in most situations, so outsiders and healthcare workers are normally not infected (except
with the most infective individuals such as those in the most progressed lepromatous forms, as those patients have the
highest bacterial loads).
LEPROSY
Leprosy, also known as Hansen's disease (HD), is a long-term infection by the bacterium Mycobacterium leprae or
Mycobacterium lepromatosis. Initially, infections are without symptoms and typically remain this way for 5 to 20 years.
Symptoms that develop include granulomas of the nerves, respiratory tract, skin, and eyes. This may result in a lack of ability
to feel pain, thus loss of parts of extremities due to repeated injuries or infection due to unnoticed wounds. Weakness and
poor eyesight may also be present.
Signs and symptoms

Leprosy is mostly a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions
(light or dark patches) are the primary external sign. If untreated, leprosy can progress and cause permanent damage to the
skin, nerves, limbs, and eyes. Secondary infections, in turn, can result in tissue loss, causing fingers and toes to become
shortened and deformed, as cartilage is absorbed into the body.

FUNGAL SKIN INFECTIONS
CANDIDIASIS
Candidiasis is a fungal infection due to any type of Candida (a type of yeast). When it affects the mouth, it is commonly called
thrush. Signs and symptoms include white patches on the tongue or other areas of the mouth and throat. Other symptoms
may include soreness and problems swallowing. When it affects the vagina, it is commonly called a yeast infection. Signs and
symptoms include genital itching, burning, and sometimes a white "cottage cheese-like" discharge from the vagina. Less
commonly the penis may be affected, resulting in itchiness. Very rarely, the infection may become invasive, spreading to
other parts of the body. This may result in fevers along with other symptoms depending on the parts involved.
Signs and symptoms

Signs and symptoms of candidiasis vary depending on the area affected. Most candidal infections result in minimal
complications such as redness, itching, and discomfort, though complications may be severe or even fatal if left untreated in
certain populations. In healthy (immunocompetent) persons, candidiasis is usually a localized infection of the skin, fingernails
or toenails (onychomycosis), or mucosal membranes, including the oral cavity and pharynx (thrush), esophagus, and the
genitalia (vagina, penis, etc.); less commonly in healthy individuals, the gastrointestinal tract, urinary tract, and respiratory
tract are sites of candida infection.

In immunocompromised individuals, Candida infections in the esophagus occur more frequently than in healthy individuals
and have a higher potential of becoming systemic, causing a much more serious condition, a fungemia called candidemia.
Symptoms of esophageal candidiasis include difficulty swallowing, painful swallowing, abdominal pain, nausea, and vomiting.
Thrush is commonly seen in infants. It is not considered abnormal in infants unless it lasts longer than a few weeks.
Infection of the vagina or vulva may cause severe itching, burning, soreness, irritation, and a whitish or whitish-gray cottage
cheese-like discharge. Symptoms of infection of the male genitalia (balanitis thrush) include red skin around the head of the
penis, swelling, irritation, itchiness and soreness of the head of the penis, thick, lumpy discharge under the foreskin, unpleasant
odour, difficulty retracting the foreskin (phimosis), and pain when passing urine or during sex.
Common symptoms of gastrointestinal candidiasis in healthy individuals are anal itching, belching, bloating, indigestion,
nausea, diarrhea, gas, intestinal cramps, vomiting, and gastric ulcers. Perianal candidiasis can cause anal itching; the lesion
can be erythematous, papular, or ulcerative in appearance, and it is not considered to be a sexually transmissible disease.
Abnormal proliferation of the candida in the gut may lead to dysbiosis. While it is not yet clear, this alteration may be the
source of symptoms generally described as the irritable bowel syndrome, and other gastrointestinal diseases.
Treatment
Candidiasis is treated with antifungal medications; these include clotrimazole, nystatin, fluconazole, voriconazole,
amphotericin B, and echinocandins. Intravenous fluconazole or an intravenous echinocandin such as caspofungin are
commonly used to treat immunocompromised or critically ill individuals.
The 2016 revision of the clinical practice guideline for the management of candidiasis lists a large number of specific treatment
regimens for Candida infections that involve different Candida species, forms of antifungal drug resistance, immune statuses,
and infection localization and severity. Gastrointestinal candidiasis in immunocompetent individuals is treated with 100–200
mg fluconazole per day for 2–3 weeks.
TINEAS
TINEA BARBAE
Tinea barbæ (also known as "Barber's itch," "Ringworm of the beard," and "Tinea sycosis" is a fungal infection of the hair.
Tinea barbae is due to a dermatophytic infection around the bearded area of men. Generally, the infection occurs as a
follicular inflammation, or as a cutaneous granulomatous lesion, i.e. a chronic inflammatory reaction. It is one of the causes
of Folliculitis. It is most common among agricultural workers, as the transmission is more common from animal-to-human
than human-to-human. The most common causes are Trichophyton mentagrophytes and T. verrucosum.
Main symptoms that occur when affected with Tinea Barbae is pimple or blister amongst affected area, swelling and redness
around infected area, red and lumpy skin on infected area. Crusting around hairs in infected area will occur, hairs on infected
area will also be effortless to pull out. Tinea Barbae can be itchy or painful to touch but these symptoms do not always occur.

Treatment can vary with severity of the infection. Moderate cases of Tinea Barbaea can be treated with topical antifungal
medications. Topical antifungal medications will come in the form of cream, which can normally be obtained over the counter.
More serious cases of Tinea Barbae warrant an oral antifungal medication.
TINEA CAPITIS
It is a cutaneous fungal infection (dermatophytosis) of the scalp. The disease is primarily caused by dermatophytes in the
Trichophyton and Microsporum genera that invade the hair shaft. The clinical presentation is typically single or multiple
patches of hair loss, sometimes with a 'black dot' pattern (often with broken-off hairs), that may be accompanied by
inflammation, scaling, pustules, and itching. Uncommon in adults, tinea capitis is predominantly seen in pre-pubertal children,
more often boys than girls.
The disease is infectious and can be transmitted by humans, animals, or objects that harbor the fungus. The fungus can also
exist in a carrier state on the scalp, without clinical symptomatology. Treatment of tinea capitis requires an oral antifungal
agent; griseofulvin is the most commonly used drug, but other newer antimycotic drugs, such as terbinafine, itraconazole,
and fluconazole have started to gain acceptance.
TINEA CORPORIS
It is a superficial fungal infection (dermatophytosis) of the arms and legs, especially on glabrous skin; however, it may occur
on any part of the body. It is similar to other forms of tinea.
Signs and symptoms

It may have a variety of appearances; most easily identifiable are the enlarging raised red rings with a central area of clearing
(ringworm). The same appearances of ringworm may also occur on the scalp (tinea capitis), beard area (tinea barbae) or the
groin (tinea cruris, known as jock itch or dhobi itch).
Other classic features of tinea corporis include:
The edge of the rash appears elevated and is scaly to touch.
Sometimes the skin surrounding the rash may be dry and flaky.
Almost invariably, there will be hair loss in areas of the infection
Treatment
Most cases are treated by application of topical antifungal creams to the skin, but in extensive or difficult to treat cases
systemic treatment with oral medication may be required. The over-the-counter options include tolnaftate.
Among the available prescription drugs, the evidence is best for terbinafine and naftifine, but other agents may also work.
Topical antifungals are applied to the lesion twice a day for at least 3 weeks. The lesion usually resolves within 2 weeks, but
therapy should be continued for another week to ensure the fungus is completely eradicated. If there are several ringworm
lesions, the lesions are extensive, complications such as secondary infection exist, or the patient is immunocompromised, oral
antifungal medications can be used. Oral medications are taken once a day for 7 days and result in higher clinical cure rates.
The antifungal medications most commonly used are itraconazole and terbinafine.

The benefits of the use of topical steroids in addition to an antifungal is unclear. There might be a greater cure rate but no
guidelines currently recommend its addition. The effect of Whitfield's ointment is also unclear.
VIRAL SKIN INFECTIONS
MOLLUSCUM CONTAGIOSUM
Molluscum contagiosum (MC), sometimes called water warts, is a viral infection of the skin that results in small, raised, pink
lesions with a dimple in the center. They may occasionally be itchy or sore. They may occur singly or in groups. Any area of
the skin may be affected, with abdomen, legs, arms, neck, genital area, and face being most common. Onset of the lesions is
around 7 weeks after infection. It usually goes away within a year without scarring.
MC is caused by a poxvirus called the molluscum contagiosum virus (MCV). The virus is spread either by direct contact
including sexual activity or via contaminated objects such as towels. The condition can also be spread to other areas of the
body by the person themselves. Risk factors include a weak immune system, atopic dermatitis, and crowded living conditions.
Following one infection, it is possible to get reinfected. Diagnosis is typically based on the appearance.
Prevention includes hand washing and not sharing personal items. While treatment is not necessary some may wish to have
the lesions removed for cosmetic reasons or to prevent spread. Removal may occur with freezing, opening up the lesion and
scraping the inside, or laser therapy. Scraping the lesion can however result in scarring. The medication cimetidine by mouth
or podophyllotoxin cream applied to the skin may also be used.
HERPES ZOSTER
Shingles, also known as herpes zoster, is a viral disease characterized by a painful skin rash with blisters in a localized area.
Typically the rash occurs in a single, wide stripe either on the left or right side of the body or face. Two to four days before
the rash occurs there may be tingling or local pain in the area. Otherwise there are typically few symptoms though some may
have fever, headache, or feel tired. The rash usually heals within two to four weeks; however, some people develop ongoing
nerve pain which can last for months or years, a condition called postherpetic neuralgia. In those with poor immune function
the rash may occur widely. If the rash involves the eye, vision loss may occur.
Shingles is due to a reactivation of varicella zoster virus (VZV) within a person's body. The disease chickenpox is caused by
the initial infection with VZV. Once chickenpox has resolved, the virus may remain inactive in nerve cells. When it reactivates,
it travels from the nerve body to the endings in the skin, producing blisters. Risk factors for reactivation include old age, poor
immune function, and having had chickenpox before 18 months of age. How the virus remains in the body or subsequently
re-activates is not well understood. Exposure to the virus in the blisters can cause chickenpox in someone who has not had
it, but will not trigger shingles. Diagnosis is typically based on a person's signs and symptoms. Varicella zoster virus is not the
same as herpes simplex virus; however, they belong to the same family of viruses.

The shingles vaccine reduces the risk of shingles by 50 to 90% depending on the vaccine used. It also decreases rates of
postherpetic neuralgia, and if shingles occurs, its severity. If shingles develops, antiviral medications such as aciclovir can
reduce the severity and duration of disease if started within 72 hours of the appearance of the rash. Evidence does not show
a significant effect of antivirals or steroids on rates of postherpetic neuralgia. Paracetamol, NSAIDs, or opioids may be used
to help with the acute pain
PARASITIC SKIN INFECTIONS
CREEPING ERUPTION
Creeping eruption is a skin infection caused by hookworms. The infection is also called cutaneous larva migrans or sandworm
disease.
Creeping eruption causes severe itching, blisters, and a red growing, winding rash. The rash can grow up to 1 to 2 centimeters
per day. The infection usually appears on areas of the body that have been exposed to the contaminated ground. These
include the feet, legs, buttocks, or back.
Creeping eruption is caused by hookworms. Hookworm eggs are found in the feces of dogs and cats. After the eggs hatch,
they mature into worms. The infection can be spread to people from skin contact with the worms in the feces. Hookworms
may be found in moist, sandy areas. Walking barefoot on contaminated grounds in warm climates is how most people get
this condition.
Creeping eruption may be treated with antiparasitic medicines (orally or topical creams) such as albendazole, and ivermectin,
and thiabendazole. This condition is self-limiting and will disappear over weeks to months even if not treated.
LICE
Head lice are tiny parasitic insects that can infest the skin. They live on people’s heads and feed on their blood. Head lice can
cause intense itching. There are two other types of lice: body lice and pubic lice.
Head lice are very contagious. They spread from person to person by close body contact, and by shared clothes and other
personal items. These can include things such as coats, hats, hairbrushes, and combs.
The most common symptom of head lice is itching. The itching can be very bad, especially at night. Lice or their eggs (nits)
can usually be seen on the hair, behind the ears, or on the neck. They can even be seen in the eyebrows and eyelashes.
Treatment

 Before applying treatment, it may be helpful to remove clothing that can become wet or stained during treatment.
 Apply lice medicine, also called pediculicide, according to the instructions contained in the box or printed on the label. If
the infested person has very long hair (longer than shoulder length), it may be necessary to use a second bottle. Pay
special attention to instructions on the label or in the box regarding how long the medication should be left on the hair
and how it should be washed out.
 Have the infested person put on clean clothing after treatment.
 If a few live lice are still found 8–12 hours after treatment, but are moving more slowly than before, do not retreat. The
medicine may take longer to kill all the lice. Comb dead and any remaining live lice out of the hair using a fine–toothed
nit comb.
 If, after 8–12 hours of treatment, no dead lice are found and lice seem as active as before, the medicine may not be
working. Do not retreat until speaking with your health care provider; a different pediculicide may be necessary. If your
health care provider recommends a different pediculicide, carefully follow the treatment instructions contained in the box
or printed on the label.
 Nit (head lice egg) combs, often found in lice medicine packages, should be used to comb nits and lice from the hair
shaft. Many flea combs made for cats and dogs are also effective.
 After each treatment, checking the hair and combing with a nit comb to remove nits and lice every 2–3 days may decrease
the chance of self–reinfestation. Continue to check for 2–3 weeks to be sure all lice and nits are gone. Nit removal is not
needed when treating with spinosad topical suspension.
 Retreatment is meant to kill any surviving hatched lice before they produce new eggs. For some drugs, retreatment is
recommended routinely about a week after the first treatment (7–9 days, depending on the drug) and for others only if
crawling lice are seen during this period. Retreatment with lindane shampoo is not recommended.
SCABIES
Scabies is an infestation of mites (tiny insects) characterized by small, red bumps and intense itching. This highly contagious
infection often spreads from person to person while they are sleeping together in the same bed, or during close, personal
contact. The itching is caused by the mites burrowing into the skin where they lay eggs that hatch a few days later. Scabies
can affect people of all ages and social classes. It is common all over the world. Scabies happens mostly in children and young
adults.
It may take between 4 to 6 weeks for a person to develop symptoms of scabies after coming in contact with an infected
person.
In children younger than 2 years of age, the lesions caused by the mites tend to happen on the head, neck, palms, and soles.
In older children and adults, the lesions are usually on the hands, between the fingers, wrists, belt line, thighs, belly button, in
the groin area, around the breasts, and in the armpits. The following are the most common symptoms of scabies. However,
each individual may experience symptoms differently. Symptoms may include:
 Itching, usually severe
 Rash, with small pimples or red bumps
 Scaly or crusty skin (with advanced conditions)
The symptoms of scabies may resemble other skin conditions. Always talk with your healthcare provider for a diagnosis.

Treatment
Scabicide lotion or cream should be applied to all areas of the body from the neck down to the feet and toes. In addition,
when treating infants and young children, scabicide lotion or cream also should be applied to their entire head and neck
because scabies can affect their face, scalp, and neck, as well as the rest of their body. Only permethrin or sulfur ointment
may be used in infants. The lotion or cream should be applied to a clean body and left on for the recommended time before
washing it off. Clean clothing should be worn after treatment. Both sexual and close personal contacts who have had direct
prolonged skin-to-skin contact with an infested person within the preceding month should be examined and treated. All
persons should be treated at the same time to prevent reinfestation.
 Permethrin cream, 5 percent (Elimite). Permethrin is a topical cream that contains chemicals that kill scabies mites and
their eggs. It is generally considered safe for adults, pregnant women, and children ages 2 months and older. This
medicine is not recommended for nursing mothers.
 Lindane lotion. This medication — also a chemical treatment — is recommended only for people who can't tolerate other
approved treatments, or for whom other treatments didn't work. This medication isn't safe for children younger than age
2 years, women who are pregnant or nursing, the elderly, or anyone who weighs less than 110 pounds (50 kilograms).
 Crotamiton (Eurax). This medication is available as a cream or a lotion. It's applied once a day for two days. This
medication isn't recommended for children or for women who are pregnant or nursing. Frequent treatment failure has
been reported with crotamiton.
 Ivermectin (Stromectol). Doctors may prescribe this oral medication for people with altered immune systems, for people
who have crusted scabies, or for people who don't respond to the prescription lotions and creams. Ivermectin isn't
recommended for women who are pregnant or nursing, or for children who weigh less than 33 pounds (15 kg).

4. DISTURBANCES IN PIGMENTATION
Pigmentation disorders involve hypopigmentation, depigmentation, or hyperpigmentation. Areas may be focal or diffuse. In
hypopigmentation, pigment is decreased, whereas in depigmentation, pigment is completely lost, leaving white skin.
Focal hypopigmentation is most commonly a consequence of

 Injury
 Inflammatory dermatoses (eg, atopic dermatitis, psoriasis)
 Burns
 Chemical exposure (especially to hydroquinones and phenols)
Focal hypopigmentation or depigmentation is also a feature of vitiligo (which may involve large areas of skin), leprosy,
nutritional deficiencies (kwashiorkor), and genetic conditions (eg, tuberous sclerosis, piebaldism, Waardenburg syndrome).
Diffuse hypopigmentation or depigmentation is most often caused by

 Albinism
 Vitiligo
Hyperpigmentation typically occurs after inflammation due to various causes. This postinflammatory hyperpigmentation is
usually focal in distribution. Hyperpigmentation may also be caused by a systemic disorder, drug, or cancer; distribution is
usually more diffuse.
VITILIGO
ETIOLOGY
Etiology is unclear, but melanocytes are lacking in affected areas. Proposed mechanisms include autoimmune destruction of
melanocytes, reduced survival of melanocytes, and primary melanocyte defects.
Vitiligo can be familial (autosomal dominant with incomplete penetrance and variable expression) or acquired. Some patients
have antibodies to melanin. Up to 30% have other autoimmune antibodies (to thyroglobulin, adrenal cells, and parietal cells)
or clinical autoimmune endocrinopathies (Addison disease, diabetes mellitus, pernicious anemia, and thyroid dysfunction).
However, the relationship is unclear and may be coincidental. The strongest association is with hyperthyroidism (Graves
disease) and hypothyroidism (Hashimoto thyroiditis).
SYMPTOMS AND SIGNS

Vitiligo is characterized by hypopigmented or depigmented areas, usually sharply demarcated and often symmetric.
Depigmentation may be localized, involving 1 or 2 spots or entire body segments (segmental vitiligo); rarely, it may be
generalized, involving most of the skin surface (universal vitiligo). However, vitiligo most commonly involves the face
(especially around the orifices), digits, dorsal hands, flexor wrists, elbows, knees, shins, dorsal ankles, armpits, inguinal area,

anogenital area, umbilicus, and nipples. Cosmetic disfigurement can be especially severe and emotionally devastating in dark-
skinned patients. Hair in vitiliginous areas is usually white.
DIAGNOSIS: CLINICAL EVALUATION

Depigmented skin is typically obvious on examination. Subtle hypopigmented or depigmented lesions are accentuated under
a Wood light. Differential diagnosis includes postinflammatory hypopigmentation, piebaldism (a rare autosomal dominant
disorder in which depigmented patches surrounded by hyperpigmented areas occur most often on the forehead, neck,
anterior trunk, and mid-extremities), morphea (localized scleroderma, in which skin is usually sclerotic), leprosy (in which
lesions are usually hypoesthetic), lichen sclerosus, pityriasis alba, chemical leukoderma, and leukoderma due to melanoma.
Although there are no evidence-based guidelines, it is reasonable for physicians to do CBC, fasting blood glucose, and thyroid
function tests.
TREATMENT
 Protection of affected areas from sunlight
 Topical corticosteroids and calcipotriene: Traditional first-line therapy is potent topical corticosteroids, which may cause
hypopigmentation or atrophy in normal surrounding skin. Calcineurin inhibitors (tacrolimus and pimecrolimus) may be
particularly useful for treating areas of the skin (such as the face and groin) where adverse effects of topical corticosteroid
therapy most commonly occur. Calcipotriene blended with betamethasone dipropionate may also be helpful and more
successful than monotherapy with either drug.
 Topical calcineurin inhibitors with face or groin involvement
 Narrowband UVB or psoralen plus ultraviolet A (PUVA) therapy: Oral and topical PUVA is often successful, but hundreds
of treatment sessions may be necessary. Narrowband UVB is as effective as topical PUVA and has few adverse effects,
making narrowband UVB preferable to PUVA. Narrowband UVB is often the preferred initial treatment for widespread
vitiligo. Excimer laser may be useful, particularly for localized disease that does not respond to initial topical therapy.
 Depigmentation of unaffected skin to achieve homogeneous skin tone is possible with 20% monobenzyl ether of
hydroquinone applied twice daily. This treatment is indicated only when most of the skin is involved and the patient is
prepared for permanent pigment loss and the subsequent increased risks of photo-induced skin damage (eg, skin
cancers, photoaging). This treatment can be extremely irritating, so a smaller test area should be treated before
widespread use. Treatment for ≥ 1 yr may be required.

5. BLISTERING DISEASES
Pemphigus is a rare group of blistering autoimmune diseases that affect the skin and mucous membranes. The name is
derived from the Greek root "pemphix" meaning "pustule".
In pemphigus, autoantibodies form against desmoglein. Desmoglein forms the "glue" that attaches adjacent epidermal cells
via attachment points called desmosomes. When autoantibodies attack desmogleins, the cells become separated from each
other and the epidermis becomes "unglued", a phenomenon called acantholysis. This causes blisters that slough off and turn
into sores. In some cases, these blisters can cover a significant area of the skin.
TYPES
There are several types of pemphigus which vary in severity: pemphigus vulgaris, pemphigus foliaceus, Intraepidermal
neutrophilic IgA dermatosis, and paraneoplastic pemphigus.
 Pemphigus vulgaris (PV - ICD-10 L10.0) is the most common form of the disorder and occurs when antibodies attack
Desmoglein 3. Sores often originate in the mouth, making eating difficult and uncomfortable. Although pemphigus
vulgaris may occur at any age, it is most common among people between the ages of 40 and 60. It is more frequent
among Ashkenazi Jews. Rarely, it is associated with myasthenia gravis. Nail disease may be the only finding and has
prognostic value in management.
 Pemphigus foliaceus (PF) is the least severe of the three varieties. Desmoglein 1, the protein that is destroyed by the
autoantibody, is found in only the top dry layer of the skin. PF is characterized by crusty sores that often begin on the
scalp, and may move to the chest, back, and face. Mouth sores do not occur. This form is also frequent among Ashkenazi
Jews. It is not as painful as pemphigus vulgaris, and is often mis-diagnosed as dermatitis or eczema
 Intraepidermal neutrophilic IgA dermatosis is characterized histologically by intraepidermal bullae with neutrophils, some
eosinophils, and acantholysis.
 The least common and most severe type of pemphigus is paraneoplastic pemphigus (PNP). This disorder is a complication
of cancer, usually lymphoma and Castleman's disease. It may precede the diagnosis of the tumor. Painful sores appear
on the mouth, lips, and the esophagus. In this variety of pemphigus, the disease process often involves the lungs, causing
bronchiolitis obliterans (constrictive bronchiolitis). Though much less frequent, it is still found the most in the Ashkenazi
Jewish population. Complete removal of and/or cure of the tumor may improve the skin disease, but lung damage is
generally irreversible.
 Endemic pemphigus foliaceus, including the Fogo Selvagem, the new variant of endemic pemphigus folaiceus in El Bagre,
Colombia, South America, and the Tunisian endemic pemphigus in North Africa.
 Bullous pemphigoid is an acute or chronic autoimmune skin disease, involving the formation of blisters, more
appropriately known as bullae, at the space between the epidermis and dermis skin layers. It is classified as a type II
hypersensitivity reaction, with the formation of anti-hemidesmosome antibodies. Clinically, the earliest lesions may
appear urticarial (like hives), but could also appear dermatitic, targetoid, lichenoid, nodular, or even without visible rash
(essential pruritus). Tense bullae eventually erupt, most commonly at the inner thighs and upper arms, but the trunk and
extremities are frequently both involved. Any part of the skin surface can be involved. Oral lesions are present in a minority
of cases.

Note that Hailey-Hailey disease, also called familial benign pemphigus, is an inherited (genetic) skin disease, not an
autoimmune disease. It is therefore not considered part of the Pemphigus group of diseases.
DIAGNOSIS
Pemphigus defines a group of autoimmune interepithelial blistering diseases that are characterized by loss of normal cell-
cell adhesion (acantholysis), and by the presence of pathogenic (predominantly IgG) autoantibodies reacting against epithelial
adhesion molecules. Pemphigus is further divided in two major subtypes: pemphigus vulgaris (PV) and pemphigus foliaceus
(PF). However, several other disorders such as IgA pemphigus, IgE pemphigus, pemphigus herpetiformis, drug induced
pemphigus, Senear Usher syndrome and endemic pemphigus foliaceus exist;recognized by a dermatologist from the
appearance and distribution of the skin lesions. It is also commonly diagnosed by specialists practicing otolaryngology- head
and neck surgery, periodontists, oral and maxillofacial surgeons and eye doctors, as lesions can affect the eyes and mucous
membrane of the oral cavity. Intraorally it resembles the more common diseases lichen planus and mucous membrane
pemphigoid. Definitive diagnosis requires examination of a skin or mucous membrane biopsy by a dermatopathologist or
oral pathologist. The skin biopsy is taken from the edge of a blister, prepared for histopathology and examined with a
microscope. The pathologist looks for an intraepidermal vesicle caused by the breaking apart of epidermal cells (acantholysis).
Thus, the superficial (upper) portion of the epidermis sloughs off, leaving the bottom layer of cells on the "floor" of the blister.
This bottom layer of cells is said to have a "tombstone appearance".
Definitive diagnosis also requires the demonstration of anti-desmoglein autoantibodies by direct immunofluorescence on
the skin biopsy. These antibodies appear as IgG deposits along the desmosomes between epidermal cells, a pattern
reminiscent of chicken wire. Anti-desmoglein antibodies can also be detected in a blood sample using the ELISA technique.
TREATMENT
If not treated, pemphigus can be fatal, usually from overwhelming opportunistic infection of lesions. The most common
treatment is the administration of oral steroids, especially prednisone, often in high doses. The side effects of corticosteroids
may require the use of so-called steroid-sparing or adjuvant drugs. One of the most dangerous side effects of high dosage
steroid treatments is intestinal perforations, which may lead to sepsis. Steroids and other medications being taken to treat
Pemphigus may also mask the effects of the perforations. Patients on high dosages of oral steroids should closely monitor
their GI health. As lesions are usually terribly painful, it is likely that pain medication can complicate and exacerbate the GI
issues caused by steroids.
Treatment options
 topical steroids, such as clobetasol
 intralesional injection of steroids, such as dexamethasone
 immunosuppressant drugs, such as CellCept (mycophenolic acid)
 serum or plasma pooled products, like Intravenous gamma globulin (IVIG) may be useful in severe cases, especially
paraneoplastic pemphigus
 biologics such as Rituximab, an anti-CD20 antibody, which was found to improve otherwise severe cases of
recalcitrant Pemphigus vulgaris.

All of these drugs may cause severe side effects, so the patient should be closely monitored by doctors. Once the outbreaks
are under control, dosage is often reduced, to lessen side effects.
If skin lesions do become infected, antibiotics may be prescribed. Tetracycline antibiotics have a mildly beneficial effect on
the disease and are sometimes enough for Pemphigus Foliaceus. In addition, talcum powder is helpful to prevent oozing
sores from adhering to bedsheets and clothes. Wound care and treatment is often akin to that used in burn units, including
careful use of dressings that don't stick to the wounds, etc.
If paraneoplastic pemphigus is diagnosed with pulmonary disease, a powerful cocktail of immune suppressant drugs is
sometimes used in an attempt to halt the rapid progression of bronchiolitis obliterans, including methylprednisolone,
ciclosporin, azathioprine, and thalidomide. Plasmapheresis may also be useful.

6. DRUG REACTIONS
ETIOLOGY
Drugs precipitate over 50% of SJS cases and up to 95% of TEN cases. The most common drug causes include
 Sulfa drugs (eg, cotrimoxazole, sulfasalazine)
 Other antibiotics (eg, aminopenicillins [usually ampicillin or amoxicillin], fluoroquinolones, cephalosporins)
 Antiepileptics (eg, phenytoin, carbamazepine, phenobarbital, valproate, lamotrigine)
 Miscellaneous individual drugs (eg, piroxicam, allopurinol, chlormezanone)
 Cases that are not caused by drugs are attributed to
 Infection (mostly with Mycoplasma pneumoniae)
 Vaccination
 Graft-vs-host disease
Rarely, a cause cannot be identified.
PATHOPHYSIOLOGY
The exact mechanism of Stevens-Johnson syndrome and toxic epidermal necrolysis is unknown; however, one theory holds
that altered drug metabolism (eg, failure to clear reactive metabolites) in some patients triggers a T-cell–mediated cytotoxic
reaction to drug antigens in keratinocytes. CD8+ T cells have been identified as important mediators of blister formation.
Recent findings suggest that granulysin released from cytotoxic T cells and natural killer cells might play a role in keratinocyte
death; granulysin concentration in blister fluid correlates with severity of disease. Another theory is that interactions between
Fas (a cell-surface receptor that induces apoptosis) and its ligand, particularly a soluble form of Fas ligand released from
mononuclear cells, lead to cell death and blister formation. A genetic predisposition for SJS/TEN has been suggested.
DIFFERENTIAL DIAGNOSIS
Differential diagnosis in Stevens-Johnson syndrome and early toxic epidermal necrolysis includes erythema multiforme, viral
exanthems, and other drug rashes; SJS/TEN can usually be differentiated clinically as the disorder evolves and is characterized
by significant pain and skin sloughing. In later stages of TEN, differential diagnosis includes the following:
 Toxic shock syndrome (usually has more prominent multiple organ involvement and different cutaneous
manifestations, such as macular rash on palms and soles that evolves to desquamation over about 2 wk)
 Exfoliative erythroderma (usually spares mucous membranes and is not as painful)
 Paraneoplastic pemphigus (sometimes with different mucocutaneous findings or in patients with evidence of cancer)
 In children, TEN is less common and must be distinguished from staphylococcal scalded skin syndrome, usually by
noting sparing of mucous membranes and risk factors, such as drug history and clinical suspicion of staphylococcal
infection.

STEVENS-JOHNSONS SYNDROME (SJS)
SIGNS AND SYMPTOMS
SJS usually begins with fever, sore throat, and fatigue, which is commonly misdiagnosed and therefore treated with antibiotics.
SJS, SJS/TEN, and TEN are often heralded by fever, sore throat, cough, and burning eyes for 1 to 3 days. Patients with these
disorders frequently experience burning pain of their skin at the start of disease. Ulcers and other lesions begin to appear in
the mucous membranes, almost always in the mouth and lips, but also in the genital and anal regions. Those in the mouth
are usually extremely painful and reduce the patient's ability to eat or drink. Conjunctivitis occurs in about 30% of children
who develop SJS. A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet,
but usually not the scalp.
SJS may be caused by adverse effects of the drugs vancomycin, allopurinol, valproate, levofloxacin, diclofenac, etravirine,
isotretinoin, fluconazole, valdecoxib, sitagliptin, oseltamivir, penicillins, barbiturates, sulfonamides, phenytoin, azithromycin,
oxcarbazepine, zonisamide, modafinil, lamotrigine, nevirapine, pyrimethamine, ibuprofen, ethosuximide, carbamazepine,
bupropion, telaprevir, and nystatin.
The second most common cause of SJS and TEN is infection, particularly in children. This includes upper respiratory infections,
otitis media, pharyngitis, and Epstein-Barr virus, Mycoplasma pneumoniae and cytomegalovirus infections. The routine use
of medicines such as antibiotics, antipyretics and analgesics to manage infections can make it difficult to identify if cases were
caused by the infection or medicines taken.
TREATMENT
SJS constitutes a dermatological emergency. Patients with documented Mycoplasma infections can be treated with oral
macrolide or oral doxycycline.
Initially, treatment is similar to that for patients with thermal burns, and continued care can only be supportive (e.g.
intravenous fluids and nasogastric or parenteral feeding) and symptomatic (e.g., analgesic mouth rinse for mouth ulcer).
Dermatologists and surgeons tend to disagree about whether the skin should be debrided.
Beyond this kind of supportive care, no treatment for SJS is accepted. Treatment with corticosteroids is controversial. Early
retrospective studies suggested corticosteroids increased hospital stays and complication rates. No randomized trials of
corticosteroids were conducted for SJS, and it can be managed successfully without them.
Other agents have been used, including cyclophosphamide and ciclosporin, but none has exhibited much therapeutic success.
Intravenous immunoglobulin treatment has shown some promise in reducing the length of the reaction and improving
symptoms. Other common supportive measures include the use of topical pain anesthetics and antiseptics, maintaining a
warm environment, and intravenous analgesics.
An ophthalmologist should be consulted immediately, as SJS frequently causes the formation of scar tissue inside the eyelids,
leading to corneal vascularization, impaired vision, and a host of other ocular problems. Those with chronic ocular surface
disease caused by SJS may find some improvement with PROSE treatment (prosthetic replacement of the ocular surface
ecosystem treatment).

PROGNOSIS
SJS (with less than 10% of body surface area involved) has a mortality rate of around 5%. The mortality for toxic epidermal
necrolysis (TEN) is 30–40%. The risk for death can be estimated using the SCORTEN scale, which takes a number of prognostic
indicators into account. It is helpful to calculate a SCORTEN within the first 3 days of hospitalization. Other outcomes include
organ damage/failure, cornea scratching, and blindness. Restrictive lung disease may develop in patients with SJS and TEN
after initial acute pulmonary involvement. Patients with SJS or TEN caused by a drug have a better prognosis the earlier the
causative drug is withdrawn.
TOXIC EPIDERMAL NECROLYSIS (TEN)

Toxic epidermal necrolysis (TEN) is a type of severe skin reaction. Together with Stevens–Johnson syndrome (SJS) it forms a
spectrum of disease, with TEN being more severe. Early symptoms include fever and flu-like symptoms. A few days later the
skin begins to blister and peel forming painful raw areas. Mucous membranes, such as the mouth, are also typically involved.
Complications include dehydration, sepsis, pneumonia, and multiple organ failure.
The most common cause is certain medications such as lamotrigine, carbamazepine, allopurinol, sulfonamide antibiotics, and
nevirapine. Other causes can include infections such as Mycoplasma pneumoniae and cytomegalovirus or the cause may
remain unknown. Risk factors include HIV/AIDS and systemic lupus erythematosus. Diagnosis is based on a skin biopsy and
involvement of more than 30% of the skin. TEN is a type of severe cutaneous adverse reactions (SCARs), together with SJS, a
SJS/TEN, and drug reaction with eosinophilia and systemic symptoms. It is called SJS when less than 10% of the skin is involved
and an intermediate form with 10 to 30% involvement. Erythema multiforme (EM) is generally considered a separate condition.
Treatment typically takes place in hospital such as in a burn unit or intensive care unit. Efforts include stopping the cause,
pain medication, and antihistamines. Antibiotics, intravenous immunoglobulins, and corticosteroids may also be used.
Treatments do not typically change the course of the underlying disease. Together with SJS it affects 1 to 2 persons per million
per year. It is more common in females than males. Typical onset is over the age of 40. Skin usually regrows over two to three
weeks; however, recovery can take months and most are left with chronic problems.
ERYTHEMA MULTIFORME
Erythema multiforme (EM) is a skin condition of unknown cause; it is a type of erythema possibly mediated by deposition of
immune complexes (mostly IgM-bound complexes) in the superficial microvasculature of the skin and oral mucous membrane
that usually follows an infection or drug exposure. It is an uncommon disorder, with peak incidence in the second and third
decades of life.
Consensus classification:
 Erythema multiforme minor—typical targets or raised, edematous papules distributed acrally
 Erythema multiforme major—typical targets or raised, edematous papules distributed acrally with involvement of
one or more mucous membranes; epidermal detachment involves less than 10% of total body surface area (TBSiA)

The mild form usually presents with mildly itchy (but itching can be very severe), pink-red blotches, symmetrically arranged
and starting on the extremities. It often takes on the classical "target lesion" appearance, with a pink-red ring around a pale
center. Resolution within 7–10 days is the norm.
Individuals with persistent (chronic) erythema multiforme will often have a lesion form at an injury site, e.g. a minor scratch
or abrasion, within a week. Irritation or even pressure from clothing will cause the erythema sore to continue to expand along
its margins for weeks or months, long after the original sore at the center heals.
Many suspected aetiologic factors have been reported to cause EM

 Infections: Bacterial (including Bacillus Calmette-Guérin (BCG) vaccination, haemolytic Streptococci, legionellosis, leprosy,
Neisseria meningitidis, Mycobacterium, Pneumococcus, Salmonella species, Staphylococcus species, Mycoplasma
pneumoniae), Chlamydial.
 Fungal (Coccidioides immitis)
 Parasitic (Trichomonas species, Toxoplasma gondii),
 Viral (especially Herpes simplex)
 Drug reactions, most commonly to: antibiotics (including, sulphonamides, penicillin), anticonvulsants (phenytoin,
barbiturates), aspirin, antituberculoids, and allopurinol and many others.
 Physical factors: radiotherapy, cold, sunlight
 Others: collagen diseases, vasculitides, non-Hodgkin lymphoma, leukaemia, multiple myeloma, myeloid metaplasia,
polycythemia

7.CUTANEOUS MANIFESTATIONS OF SYSTEMIC
DISEASES
SISTER MARY JOSEPH NODULE
the Sister Mary Joseph nodule or more commonly node, also called Sister Mary Joseph sign, refers to a palpable nodule
bulging into the umbilicus as a result of metastasis of a malignant cancer in the pelvis or abdomen. Sister Mary Joseph
nodules can be painful to palpation.
Gastrointestinal malignancies account for about half of underlying sources (most commonly gastric cancer, colonic cancer or
pancreatic cancer, mostly of the tail and body of the pancreas), and men are even more likely to have an underlying cancer
of the gastrointestinal tract. Gynecological cancers account for about 1 in 4 cases (primarily ovarian cancer and also uterine
cancer). Nodules will also, rarely, originate from appendix cancer spillage and pseudomyxoma peritonei. Unknown primary
tumors and rarely, urinary or respiratory tract malignancies can cause umbilical metastases. How exactly the metastases reach
the umbilicus remains largely unknown. Proposed mechanisms for the spread of cancer cells to the umbilicus include direct
transperitoneal spread, via the lymphatics which run alongside the obliterated umbilical vein, hematogenous spread, or via
remnant structures such as the falciform ligament, median umbilical ligament, or a remnant of the vitelline duct. Sister Mary
Joseph nodule is associated with multiple peritoneal metastases and a poor prognosis.
PARANEOPLASTIC SYNDROMES
A paraneoplastic syndrome is a syndrome (a set of signs and symptoms) that is the consequence of cancer in the body, but
unlike mass effect, is not due to the local presence of cancer cells. In contrast, these phenomena are mediated by humoral
factors (such as hormones or cytokines) secreted by tumor cells or by an immune response against the tumor.
The skin often presents a clue that an internal malignancy is present. The combination of a malignancy and associated signs
and symptoms that are seemingly unrelated to the actual tumor is called a “paraneoplastic” syndrome.
The following diseases manifest by means of mucocutaneous dysfunction: acanthosis nigricans, dermatomyositis, Leser-Trélat
sign, necrolytic migratory erythema, Sweet's syndrome, Florid cutaneous papillomatosis, pyoderma gangrenosum, and
acquired generalized hypertrichosis. Mucocutaneous dysfunctions of paraneoplastic syndromes can be seen in cases of
itching (hypereosinophilia), immune system depression (latent varicella-zoster virus in sensory ganglia), pancreatic tumors
(leading to adipose nodular necrosis of subcutaneous tissues, flushes (prostaglandin secretions), and even dermic melanosis
(cannot be eliminated via urine and results in grey to black-blueish skin tones).
ERYTHEMA GYRATUM REPENS

Erythema gyratum repens is rare and is the most distinctive of the gyrate erythemas. There are broad erythematous bands
arranged in an arcuate or polycyclic pattern, often accompanied by a trailing scale and likened to wood grain or marble. The
eruption, which is often pruritic, may migrate up to 1 cm per day. It is usually confined to the trunk and proximal parts of the
limbs; the face is not affected.
Erythema gyratum repens is usually associated with an internal cancer, particularly of pulmonary origin . It has been reported
in association with transitional cell carcinoma of the kidney and acquired ichthyosis. It has also been reported in association
with pulmonary tuberculosis, ichthyosis, epidermolysis bullosa acquisita associated with ulcerative colitis, and in the resolving
stage of pityriasis rubra pilaris. It also occurs in otherwise healthy individuals.
It has been suggested that lymphokines produced by the tumor, such as epidermal growth factor, may play a role in the
pathogenesis.
GLUCAGONOMA SYNDROME
A glucagonoma is a rare tumor of the alpha cells of the pancreas that results in the overproduction of the hormone glucagon.
Alpha cell tumors are commonly associated with glucagonoma syndrome, though similar symptoms are present in cases of
pseudoglucagonoma syndrome in the absence of a glucagon-secreting tumor.
Necrolytic migratory erythema (NME) is a classical symptom observed in patients with glucagonoma and is the presenting
problem in 70% of cases. Associated NME is characterized by the spread of erythematous blisters and swelling across areas
subject to greater friction and pressure, including the lower abdomen, buttocks, perineum, and groin.
Less common than NME with glucagonoma, pseudoglucagonoma syndrome may occur in a number of systemic disorders:
 Celiac disease
 Ulcerative colitis
 Crohn's disease
 Hepatic cirrhosis
 Hepatocellular carcinoma
 Lung cancer, including small cell lung cancer
 Tumors that secrete insulin- or insulin-like growth factor 2
 Duodenal cancer
SWEET’S SYNDROME (ACUTE FEBRILE NEUTROPHILIC DERMATOSIS)

It is a skin disease characterized by the sudden onset of fever, an elevated white blood cell count, and tender, red, well-
demarcated papules and plaques that show dense infiltrates by neutrophil granulocytes on histologic examination.
Acute, tender, erythematous plaques, nodes, pseudovesicles and, occasionally, blisters with an annular or arciform pattern
occur on the head, neck, legs, and arms, particularly the back of the hands and fingers. The trunk is rarely involved. Fever
(50%); arthralgia or arthritis (62%); eye involvement, most frequently conjunctivitis or iridocyclitis (38%); and oral aphthae
(13%) are associated features.

Although it may occur in the absence of other known disease, SS is often associated with hematologic disease (including
leukemia), and immunologic disease (rheumatoid arthritis, inflammatory bowel disease, Behçet's syndrome).
TROUSSEAU SIGN OF MALIGNANCY

The Trousseau sign of malignancy or Trousseau's syndrome is a medical sign involving episodes of vessel inflammation due
to blood clot (thrombophlebitis) which are recurrent or appearing in different locations over time (thrombophlebitis migrans
or migratory thrombophlebitis). The location of the clot is tender and the clot can be felt as a nodule under the skin.
Trousseau's syndrome is a rare variant of venous thromboembolism (VTE) that is characterized by recurrent, migratory
thrombosis in superficial veins and in uncommon sites, such as the chest wall and arms. This syndrome is particularly
associated with pancreatic, gastric and lung cancer and Trousseau's syndrome can be an early sign of cancer sometimes
appearing months to years before the tumor would be otherwise detected. Heparin therapy is recommended to prevent
future clots. The Trousseau sign of malignancy should not be confused with the Trousseau sign of latent tetany caused by
low levels of calcium in the blood.
PYODERMA GANGRENOSUM
It is a condition that causes tissue to become necrotic, causing deep ulcers that usually occur on the legs. When they occur,
they can lead to chronic wounds. Ulcers usually initially look like small bug bites or papules, and they progress to larger ulcers.
Though the wounds rarely lead to death, they can cause pain and scarring.
There are two main types of pyoderma gangrenosum:

 the 'typical' ulcerative form, which occurs in the legs
 an 'atypical' form that is more superficial and occurs in the hands and other parts of the body
Other variations are:

 Peristomal pyoderma gangrenosum comprises 15% of all cases of pyoderma
 Bullous pyoderma gangrenosum
 Pustular pyoderma gangrenosum
 Vegetative pyoderma gangrenosum
The following are conditions commonly associated with pyoderma gangrenosum:

a) Inflammatory bowel disease:
 Ulcerative colitis
 Crohn's disease
b) Arthritides:
 Rheumatoid arthritis
 Seronegative arthritis
c) Hematological disease:
 Myelocytic leukemia

 Hairy cell leukemia
 Myelofibrosis
 Myeloid metaplasia
 Monoclonal gammopathy
d) Autoinflammatory disease:
 Pyogenic sterile arthritis, pyoderma gangrenosum, and acne syndrome (PAPA syndrome)
CULLEN'S SIGN
It is superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus. It is named for gynecologist Thomas
Stephen Cullen (1869–1953), who first described the sign in ruptured ectopic pregnancy in 1916.
This sign takes 24–48 hours to appear and can predict acute pancreatitis, with mortality rising from 8–10% to 40%. It may be
accompanied by Grey Turner's sign (bruising of the flank), which may then be indicative of pancreatic necrosis with
retroperitoneal or intraabdominal bleeding.
Causes include:
 acute pancreatitis, where methemalbumin formed from digested blood tracks around the abdomen from the
inflamed pancreas
 bleeding from blunt abdominal trauma
 bleeding from aortic rupture
 bleeding from ruptured ectopic pregnancy
XANTHOMAS
A xanthoma, from Greek meaning 'yellow', is a deposition of yellowish cholesterol-rich material that can appear anywhere in
the body in various disease states. They are cutaneous manifestations of lipidosis in which lipids accumulate in large foam
cells within the skin. They are associated with hyperlipidemias, both primary and secondary types.
Tendon xanthomas are associated with type II hyperlipidemia, chronic biliary tract obstruction, and primary biliary cirrhosis.
Palmar xanthomata and tuboeruptive xanthomata (over knees and elbows) occur in type III hyperlipidemia.
ACANTHOSIS NIGRICANS
It is a brown to black, poorly defined, velvety hyperpigmentation of the skin. It is usually found in body folds, such as the
posterior and lateral folds of the neck, the armpits, groin, navel, forehead, and other areas.
Acanthosis nigricans is conventionally divided into benign and malignant forms, although may be divided into syndromes
according to cause:
 Benign This may include obesity-related, hereditary, and endocrine forms of acanthosis nigricans.
 Malignant. This may include forms that are associated with tumour products and insulin-like activity, or tumour
necrosis factor.
An alternate classification system still used to describe acanthosis nigricans was proposed in 1994. It delineates acanthosis
nigricans syndromes according to their associated syndromes, including benign and malignant forms, forms associated with
obesity and drugs, acral acanthosis nigricans, unilateral acanthosis nigricans, and mixed and syndromic forms.

It typically occurs in individuals younger than age 40, may be genetically inherited, and is associated with obesity or
endocrinopathies, such as hypothyroidism, acromegaly, polycystic ovary disease, insulin-resistant diabetes, or Cushing's
disease.
ERYTHEMA NODOSUM
Also known as subacute migratory panniculitis of Vilanova and Piñol, is an inflammatory condition characterized by
inflammation of the fat cells under the skin, resulting in tender red nodules or lumps that are usually seen on both shins. It
can be caused by a variety of conditions, and typically resolves spontaneously within 30 days. It is common in young people
between 12–20 years of age.
Associated conditions
 Infections: Streptococcal infection which, in children, is by far the most common precipitant, Primary infection of
Tuberculosis, Mycoplasma pneumoniae, Histoplasma capsulatum, Yersinia, Epstein-Barr virus, Coccidioides immitis
(Valley fever), Cat scratch disease
 Autoimmune disorders, including Inflammatory bowel disease (IBD), Behçet's disease, Sarcoidosis
 Pregnancy
 Medications, including Sulfonamides, Penicillins, Oral contraceptives, Bromides, Hepatitis B vaccination
 Cancer, including Non-Hodgkins lymphoma (NHL), Carcinoid tumours, Pancreatic cancer
DERMATOLOGIC MANIFESTATIONS OF LIVER DISEASE

 Vascular: Spider telangiectasia, Palmer erythema, Corkscrew scleral vessels, Caput medusae, Plethoric facies, Flushing,
Unilateral nevoid telangiectasia.
 Jaundice: Pruritus, Urticaria,
 Nail changes: Koilonychia, Clubbing.
 Hyperpigmentation
 Skin cancer
 Lichenoid dermatitis
SKIN MANIFESTATIONS OF RENAL DISEASES

 Uremic pruritus :generalized or localized excoriations, lesions of lichen simplex chronicus, and prurigo nodularis.
Mediated by various chemical mediators neurotransmitters: (pentapeptide enkephalins, proteases, serotonin, and
histamine..)
 Xerosis : the dry or roughened skin texture. A direct relation between xerosis and stratum corneum water content. A
thicker though fractured stratum corneum leads to increase transepidermal water loss.
 Cutaneous pigmentation: pallor, brown-to-slate-gray discoloration, yellowish (sallow) hue, and brownish
hyperpigmentation in sun-exposed areas. Due to increased levels of melanocyte stimulating hormone (MSH).
 Calciphylaxis: a life-threatening condition of progressive cutaneous necrosis due to small- and medium-sized vessel
calcification. A complication of secondary hyperparathyroidism in chronic renal failure. Firm, bilaterally symmetric non-

ulcerating painful pre-infarctive ischemic plaques that appear as mottling or violaceous discoloration on the extremities
developing into necrotic areas. Flaccid or hemorrhagic bullae may form over ischemic tissue.
DIABETES MELLITUS
 Vascular microangiopathies and rubeosis
 Recurrent skin infections: either due to fungi (e.g. genital candidiasis) or bacteria (e.g. folliculitis).
 Blisters on the feet
 Wet gangrenes
 Peripheral neuropathy and trophic skin changes
 Brown macules sometimes develop on the shin
 Plaques with dark red or purple edges, atrophic centres, and surface telangectasia (Necrobiosis lipoidica diabeticorum
)

8. ICTHYOSIS
Ichthyosis is a family of rare genetic skin disorders characterized by dry, thickened, scaly skin.
There are more than 20 types of ichthyosis which range in severity of symptoms, outward appearance, underlying genetic
cause and mode of inheritance (e.g., whether the abnormal gene inherited is dominant, recessive, autosomal or X-linked).
Ichthyosis comes from the Greek ἰχθύς, ichthys, literally "fish", since dry, scaly skin is the defining feature of all forms of
ichthyosis.
The severity of symptoms can vary enormously, from the mildest, most common, types such as ichthyosis vulgaris, which may
be mistaken for normal dry skin, up to life-threatening conditions such as harlequin type ichthyosis. Ichthyosis vulgaris
accounts for more than 95% of cases.
Ichthyosis vulgaris (also known as "Autosomal dominant ichthyosis," and "Ichthyosis simplex") is a skin disorder causing dry,
scaly skin. It is the most common form of ichthyosis, affecting around 1 in 250 people. For this reason it is known as common
ichthyosis. It is usually an autosomal dominant inherited disease (often associated with filaggrin), although a rare non-
heritable version called acquired ichthyosis exists. The symptoms of the inherited form of ichthyosis vulgaris are not usually
present at birth but generally develop between 3 months and 5 years of age. The symptoms will often improve with age,
although they may grow more severe again in old age. The condition is not life-threatening; the impact on the patient, if it is

a mild case, is generally restricted to mild itching and the social impact of having skin with an unusual appearance. People
with mild cases have symptoms that include scaly patches on the shins, fine white scales on the forearms and upper arms,
and rough palms. People with the mildest cases have no symptoms other than faint, tell-tale "mosaic lines" between the
Achilles tendons and the calf muscles.
X-linked ichthyosis (XLI) (also known as ") is a skin condition caused by the hereditary deficiency of the steroid sulfatase (STS)
enzyme that affects 1 in 2000 to 1 in 6000 males. XLI manifests with dry, scaly skin and is due to deletions or mutations in the
STS gene. XLI can also occur in the context of larger deletions causing contiguous gene syndromes. Treatment is largely
aimed at alleviating the skin symptoms. The term is from the Ancient Greek 'ichthys' meaning 'fish'.
Epidermolytic hyperkeratosis is a skin disorder that is present at birth. Affected babies may have very red skin (erythroderma)
and severe blisters. Because newborns with this disorder are missing the protection provided by normal skin, they are at risk
of becoming dehydrated and developing infections in the skin or throughout the body (sepsis). As affected individuals get
older, blistering is less frequent, erythroderma becomes less evident, and the skin becomes thick (hyperkeratotic), especially
over joints, on areas of skin that come into contact with each other, or on the scalp or neck. This thickened skin is usually
darker than normal. Bacteria can grow in the thick skin, often causing a distinct odor.
Harlequin-type ichthyosis is a genetic disorder which results in thickened skin over nearly the entire body at birth. The skin
forms large, diamond-shaped plates that are separated by deep cracks. They affect the shape of the eyelids, nose, mouth,
and ears, and limit movement of the arms and legs. Restricted movement of the chest can lead to breathing difficulties. These
plates fall off over weeks. Other complications can include premature birth, infection, problems with body temperature, and
dehydration. Harlequin-type ichthyosis is due to mutations of the ABCA12 genes. It is inherited from a person's parents in an
autosomal recessive manner. Diagnosis is often based on appearance at birth and confirmed by genetic testing. Before birth
amniocentesis or ultrasound may support the diagnosis. There is no cure. Early in life constant supportive care is typically
required. Treatments may include moisturizing cream, antibiotics, etretinate, or retinoids. It affects about 1 per 300,000 births.
Both sexes are affected equally commonly. Long term problems are common. Death in the first month is relatively common.
DIAGNOSIS
A family history is very useful. In some cases, a skin biopsy is done to help to confirm the diagnosis. In some instances, genetic
testing may be helpful in making a diagnosis. Diabetes has not been definitively linked to acquired ichthyosis or ichthyosis
vulgaris; however, there are case reports associating new onset ichthyosis with diabetes.
Ichthyosis has been found to be more common in Native American, Asian, Mongolian groups. There is no way to prevent
ichthyosis.
Ichthyosis is a genetically and phenotypically heterogeneous disease that can be isolated and restricted to the skin
manifestations or associated with extracutaneous symptoms. One of which is limb reduction defect known as CHILD
syndrome; a rare inborn error of metabolism of cholesterol biosynthesis that is usually restricted to one side of the body. A
research done in Egypt proved that it is not a child syndrome and discussed all the case report.
TREATMENT

Treatments for ichthyosis often take the form of topical application of creams and emollient oils, in an attempt to hydrate the
skin. Creams containing lactic acid have been shown to work exceptionally well in some cases. Application of propylene glycol
is another treatment method. Retinoids are used for some conditions.
Exposure to sunlight may improve or worsen the condition. In some cases, excess dead skin sloughs off much better from
wet tanned skin after bathing or a swim, although the dry skin might be preferable to the damaging effects of sun exposure.
There can be ocular manifestations of ichthyosis, such as corneal and ocular surface diseases. Vascularizing keratitis, which is
more commonly found in congenital keratitis-ichythosis-deafness (KID), may worsen with isotretinoin therapy.

9. ECZEMA
Dermatitis, also known as eczema, is a group of diseases that results in inflammation of the skin. These diseases are
characterized by itchiness, red skin, and a rash. In cases of short duration there may be small blisters while in long-term cases
the skin may become thickened. The area of skin involved can vary from small to the entire body.
SIGNS AND SYMPTOMS

Dermatitis symptoms vary with all different forms of the condition. They range from skin rashes to bumpy rashes or including
blisters. Although every type of dermatitis has different symptoms, there are certain signs that are common for all of them,
including redness of the skin, swelling, itching and skin lesions with sometimes oozing and scarring. Also, the area of the skin
on which the symptoms appear tends to be different with every type of dermatitis, whether on the neck, wrist, forearm, thigh
or ankle. Although the location may vary, the primary symptom of this condition is itchy skin. More rarely, it may appear on
the genital area, such as the vulva or scrotum. Symptoms of this type of dermatitis may be very intense and may come and
go. Irritant contact dermatitis is usually more painful than itchy.
Although the symptoms of atopic dermatitis vary from person to person, the most common symptoms are dry, itchy, red
skin. Typical affected skin areas include the folds of the arms, the back of the knees, wrists, face and hands. Perioral dermatitis
refers to a red bumpy rash around the mouth.
Dermatitis herpetiformis symptoms include itching, stinging and a burning sensation. Papules and vesicles are commonly
present. The small red bumps experienced in this type of dermatitis are usually about 1 cm in size, red in color and may be
found symmetrically grouped or distributed on the upper or lower back, buttocks, elbows, knees, neck, shoulders, and scalp.
Less frequently, the rash may appear inside the mouth or near the hairline.
The symptoms of seborrheic dermatitis, on the other hand, tend to appear gradually, from dry or greasy scaling of the scalp
(dandruff) to scaling of facial areas, sometimes with itching, but without hair loss. In newborns, the condition causes a thick
and yellowish scalp rash, often accompanied by a diaper rash. In severe cases, symptoms may appear along the hairline,
behind the ears, on the eyebrows, on the bridge of the nose, around the nose, on the chest, and on the upper back.
COMMON TYPES
Diagnosis of types may be indicated by codes defined according to International Statistical Classification of Diseases and
Related Health Problems (ICD).
Atopic
Atopic dermatitis is an allergic disease believed to have a hereditary component and often runs in families whose members
have asthma. Itchy rash is particularly noticeable on head and scalp, neck, inside of elbows, behind knees, and buttocks. It is
very common in developed countries, and rising. Irritant contact dermatitis is sometimes misdiagnosed as atopic dermatitis.
Contact

Contact dermatitis is of two types: allergic (resulting from a delayed reaction to an allergen, such as poison ivy, nickel, or
Balsam of Peru), and irritant (resulting from direct reaction to a detergent, such as sodium lauryl sulfate, for example). Some
substances act both as allergen and irritant (wet cement, for example). Other substances cause a problem after sunlight
exposure, bringing on phototoxic dermatitis. About three quarters of cases of contact eczema are of the irritant type, which
is the most common occupational skin disease. Contact eczema is curable, provided the offending substance can be avoided
and its traces removed from one's environment.
Seborrhoeic
Seborrhoeic dermatitis or seborrheic dermatitis ("cradle cap" in infants) is a condition sometimes classified as a form of
eczema that is closely related to dandruff. It causes dry or greasy peeling of the scalp, eyebrows, and face, and sometimes
trunk. In newborns it causes a thick, yellow, crusty scalp rash called cradle cap, which seems related to lack of biotin and is
often curable.
LESS COMMON TYPES

Dyshidrosis
Dyshidrosis (dyshidrotic eczema, pompholyx, vesicular palmoplantar dermatitis) only occurs on palms, soles, and sides of
fingers and toes. Tiny opaque bumps called vesicles, thickening, and cracks are accompanied by itching, which gets worse at
night. A common type of hand eczema, it worsens in warm weather.
Discoid
Discoid eczema (nummular eczema, exudative eczema, microbial eczema) is characterized by round spots of oozing or dry
rash, with clear boundaries, often on lower legs. It is usually worse in winter. Cause is unknown, and the condition tends to
come and go.
Venous
Venous eczema (gravitational eczema, stasis dermatitis, varicose eczema) occurs in people with impaired circulation, varicose
veins, and edema, and is particularly common in the ankle area of people over 50. There is redness, scaling, darkening of the
skin, and itching. The disorder predisposes to leg ulcers.
Herpetiformis
Dermatitis herpetiformis (Duhring's disease) causes intensely itchy and typically symmetrical rash on arms, thighs, knees, and
back. It is directly related to celiac disease, can often be put into remission with appropriate diet, and tends to get worse at
night.
Neurodermatitis
Neurodermatitis (lichen simplex chronicus, localized scratch dermatitis) is an itchy area of thickened, pigmented eczema patch
that results from habitual rubbing and scratching. Usually there is only one spot. Often curable through behavior modification
and anti-inflammatory medication. Prurigo nodularis is a related disorder showing multiple lumps.
Autoeczematization

Autoeczematization (id reaction, autosensitization) is an eczematous reaction to an infection with parasites, fungi, bacteria,
or viruses. It is completely curable with the clearance of the original infection that caused it. The appearance varies depending
on the cause. It always occurs some distance away from the original infection.
Viral
There are eczemas overlaid by viral infections (eczema herpeticum or vaccinatum), and eczemas resulting from underlying
disease (e.g., lymphoma). Eczemas originating from ingestion of medications, foods, and chemicals, have not yet been clearly
systematized. Other rare eczematous disorders exist in addition to those listed here.
PREVENTION
There is no good evidence that a mother's diet during pregnancy, the formula used, or breastfeeding changes the risk. There
is tentative evidence that probiotics in infancy may reduce rates but it is insufficient to recommend its use.
People with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially
severe and sometimes fatal complication.
MANAGEMENT
a) There is no known cure for some types of dermatitis, with treatment aiming to control symptoms by reducing
inflammation and relieving itching. Contact dermatitis is treated by avoiding what is causing it.
b) Lifestyle: Bathing once or more a day is recommended, usually for five to ten minutes in warm water. Soaps should be
avoided as they tend to strip the skin of natural oils and lead to excessive dryness.
c) There has not been adequate evaluation of changing the diet to reduce eczema. There is some evidence that infants with
an established egg allergy may have a reduction in symptoms if eggs are eliminated from their diets. Benefits have not
been shown for other elimination diets, though the studies are small and poorly executed. Establishing that there is a
food allergy before dietary change could avoid unnecessary lifestyle changes.
d) People can wear clothing designed to manage the itching, scratching and peeling.
e) House dust mite reduction and avoidance measures have been studied in low quality trials and have not shown evidence
of improving eczema.
f) Moisturizers: Moisturizing agents (also known as emollients) are demonstrated to decrease eczema severity and lead to
fewer flares. In children, oil based- formulations appear to be better and water-based formulations are not recommended.
It is unclear if moisturizers that contain ceramides are more or less effective than others. Products that contain dyes,
perfumes, or peanuts should not be used.[4] Occlusive dressings at night may be useful
g) Medications: There is little evidence for antihistamine; they are thus not generally recommended. Sedative antihistamines,
such as diphenhydramine, may be tried in those who are unable to sleep due to eczema.
 Colloidal oatmeal: Oatmeal contains avenanthramide (anthranilic acid amides), which can have an anti-inflammatory
effect.
 Corticosteroids: If symptoms are well controlled with moisturizers, steroids may only be required when flares occur.
Corticosteroids are effective in controlling and suppressing symptoms in most cases. Once daily use is generally
enough. For mild-moderate eczema a weak steroid may be used (e.g., hydrocortisone), while in more severe cases a
higher-potency steroid (e.g., clobetasol propionate) may be used. In severe cases, oral or injectable corticosteroids
may be used. While these usually bring about rapid improvements, they have greater side effects. Long term use of
topical steroids may result in skin atrophy, stria, telangiectasia. Their use on delicate skin (face or groin) is therefore

typically with caution. They are, however, generally well tolerated.[50] Red burning skin, where the skin turns red
upon stopping steroid use, has been reported among adults who use topical steroids at least daily for more than a
year.
h) Immunosuppressants: Topical immunosuppressants like pimecrolimus and tacrolimus may be better in the short term
and appear equal to steroids after a year of use. Their use is reasonable in those who do not respond to or are not
tolerant of steroids. Treatments are typically recommended for short or fixed periods of time rather than indefinitely.
Tacrolimus 0.1% has generally proved more effective than pimecrolimus, and equal in effect to mid-potency topical
steroids. There is no link to increased risk of cancer from topical use of 1% pimecrolimus cream.
i) Light therapy using ultraviolet light has tentative support but the quality of the evidence is not very good. A number of
different types of light may be used including UVA and UVB; in some forms of treatment, light sensitive chemicals such
as psoralen are also used. Overexposure to ultraviolet light carries its own risks, particularly that of skin cancer.

10. PSORIASIS
Psoriasis is a long-lasting autoimmune disease characterized by patches of abnormal skin. These skin patches are
typically red, itchy, and scaly. Psoriasis varies in severity from small, localized patches to complete body coverage.
Injury to the skin can trigger psoriatic skin changes at that spot, which is known as the Koebner phenomenon.
SIGNS AND SYMPTOMS

PLAQUE PSORIASIS
Psoriasis vulgaris (also known as chronic stationary psoriasis or plaque-like psoriasis) is the most common form and affects
85%–90% of people with psoriasis. Plaque psoriasis typically appears as raised areas of inflamed skin covered with silvery-
white scaly skin. These areas are called plaques and are most commonly found on the elbows, knees, scalp, and back. Psoriatic
erythroderma (erythrodermic psoriasis) involves widespread inflammation and exfoliation of the skin over most of the body
surface. It may be accompanied by severe itching, swelling, and pain. It is often the result of an exacerbation of unstable
plaque psoriasis, particularly following the abrupt withdrawal of systemic glucocorticoids. This form of psoriasis can be fatal
as the extreme inflammation and exfoliation disrupt the body's ability to regulate temperature and perform barrier functions.
PUSTULAR PSORIASIS
Characteristics may vary according to the subtype of pustular psoriasis. For example, it can be localized, commonly to the
hands and feet (localized pustular psoriasis), or generalized with widespread patches occurring randomly on any part of the
body (generalized pustular psoriasis). However, all forms of pustular psoriasis share in common the presence of red and
tender blotchy skin covered with pustules.
Pustular psoriasis can be localized, commonly to the hands and feet (palmoplantar pustulosis), or generalized with widespread
patches occurring randomly on any part of the body. Acrodermatitis continua is a form of localized psoriasis limited to the
fingers and toes that may spread to the hands and feet. Pustulosis palmaris et plantaris is another form of localized pustular
psoriasis similar to acrodermatitis continua with pustules erupting from red, tender, scaly skin found on the palms of the
hands and the soles of the feet.
Generalized pustular psoriasis (GPP) is also known as (von Zumbusch) acute generalized pustular psoriasis in acute cases,
and as impetigo herpetiformis during pregnancy. GPP is a rare and severe form of psoriasis that may require hospitalization.
This form of psoriasis is characterized by an acute onset of numerous pustules on top of tender red skin. This skin eruption
is often accompanied by a fever, muscle aches, nausea, and an elevated white blood cell count. Annular pustular psoriasis
(APP), a rare form of GPP, is the most common type seen during childhood.
INVERSE PSORIASIS
Inverse psoriasis (also known as flexural psoriasis) appears as smooth, inflamed patches of skin. The patches frequently affect
skin folds, particularly around the genitals (between the thigh and groin), the armpits, in the skin folds of an overweight
abdomen (known as panniculus), between the buttocks in the intergluteal cleft, and under the breasts in the inframammary
fold. Heat, trauma, and infection are thought to play a role in the development of this atypical form of psoriasis.

GUTTATE PSORIASIS
Guttate psoriasis is characterized by numerous small, scaly, red or pink, droplet-like lesions (papules). These numerous spots
of psoriasis appear over large areas of the body, primarily the trunk, but also the limbs and scalp. Guttate psoriasis is often
triggered by a streptococcal infection, typically streptococcal pharyngitis. The reverse is not true.
MOUTH
Psoriasis in the mouth is very rare, in contrast to lichen planus, another common papulosquamous disorder that commonly
involves both the skin and mouth. When psoriasis involves the oral mucosa (the lining of the mouth), it may be asymptomatic,
but it may appear as white or grey-yellow plaques. Fissured tongue is the most common finding in those with oral psoriasis
and has been reported to occur in 6.5–20% of people with psoriasis affecting the skin. The microscopic appearance of oral
mucosa affected by geographic tongue (migratory stomatitis) is very similar to the appearance of psoriasis. However, modern
studies have failed to demonstrate any link between the two conditions.
PSORIATIC ARTHRITIS
Psoriatic arthritis is a form of chronic inflammatory arthritis that has a highly variable clinical presentation and frequently
occurs in association with skin and nail psoriasis. It typically involves painful inflammation of the joints and surrounding
connective tissue and can occur in any joint, but most commonly affects the joints of the fingers and toes. This can result in
a sausage-shaped swelling of the fingers and toes known as dactylitis. Psoriatic arthritis can also affect the hips, knees, spine
(spondylitis), and sacroiliac joint (sacroiliitis). About 30% of individuals with psoriasis will develop psoriatic arthritis. Skin
manifestations of psoriasis tend to occur before arthritic manifestations in about 75% of cases.
CAUSES
The cause of psoriasis is not fully understood, but a number of theories exist.
a) Genetics: Around one-third of people with psoriasis report a family history of the disease, and researchers have identified
genetic loci associated with the condition. Identical twin studies suggest a 70% chance of a twin developing psoriasis if
the other twin has the disorder. The risk is around 20% for nonidentical twins. These findings suggest both a genetic
susceptibility and an environmental response in developing psoriasis.
b) Lifestyle: Conditions reported as worsening the disease include chronic infections, stress, and changes in season and
climate. Others that might worsen the condition include hot water, scratching psoriasis skin lesions, skin dryness, excessive
alcohol consumption, cigarette smoking, and obesity.
c) HIV: The rate of psoriasis in HIV-positive individuals is comparable to that of HIV-negative individuals, however, psoriasis
tends to be more severe in people infected with HIV. A much higher rate of psoriatic arthritis occurs in HIV-positive
individuals with psoriasis than in those without the infection. The immune response in those infected with HIV is typically
characterized by cellular signals from Th2 subset of CD4+ helper T cells, whereas the immune response in psoriasis
vulgaris is characterized by a pattern of cellular signals typical of Th1 subset of CD4+ helper T cells and Th17 helper T
cells. It is hypothesized that the diminished CD4+-T cell presence causes an overactivation of CD8+-T cells, which are
responsible for the exacerbation of psoriasis in HIV-positive people. Psoriasis in those with HIV/AIDS is often severe and
may be untreatable with conventional therapy.

d) Microbes: Psoriasis has been described as occurring after strep throat, and may be worsened by skin or gut colonization
with Staphylococcus aureus, Malassezia, and Candida albicans.
e) Medications: Drug-induced psoriasis may occur with beta blockers, lithium, antimalarial medications, non-steroidal anti-
inflammatory drugs, terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor,
interleukins, interferons, lipid-lowering drugs, and paradoxically TNF inhibitors such as infliximab or adalimumab.
Withdrawal of corticosteroids (topical steroid cream) can aggravate psoriasis due to the rebound effect.
MECHANISM
Psoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin. Abnormal
production of skin cells (especially during wound repair) and an overabundance of skin cells result from the sequence of
pathological events in psoriasis. Skin cells are replaced every 3–5 days in psoriasis rather than the usual 28–30 days. These
changes are believed to stem from the premature maturation of keratinocytes induced by an inflammatory cascade in the
dermis involving dendritic cells, macrophages, and T cells (three subtypes of white blood cells). These immune cells move
from the dermis to the epidermis and secrete inflammatory chemical signals (cytokines) such as interleukin-36γ, tumor
necrosis factor-α, interleukin-1β, interleukin-6, and interleukin-22. These secreted inflammatory signals are believed to
stimulate keratinocytes to proliferate. One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the
regulatory cytokine interleukin-10.
Gene mutations of proteins involved in the skin's ability to function as a barrier have been identified as markers of
susceptibility for the development of psoriasis.
DNA released from dying cells acts as an inflammatory stimulus in psoriasis and stimulates the receptors on certain dendritic
cells, which in turn produce the cytokine interferon-α. In response to these chemical messages from dendritic cells and T cells,
keratinocytes also secrete cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-α, which signal downstream
inflammatory cells to arrive and stimulate additional inflammation.
Dendritic cells bridge the innate immune system and adaptive immune system. They are increased in psoriatic lesions and
induce the proliferation of T cells and type 1 helper T cells (Th1). Targeted immunotherapy as well as psoralen and ultraviolet
A (PUVA) therapy can reduce the number of dendritic cells and favors a Th2 cell cytokine secretion pattern over a Th1/Th17
cell cytokine profile. Psoriatic T cells move from the dermis into the epidermis and secrete interferon-γ and interleukin-17.
Interleukin-23 is known to induce the production of interleukin-17 and interleukin-22. Interleukin-22 works in combination
with interleukin-17 to induce keratinocytes to secrete neutrophil-attracting cytokines.
DIAGNOSIS
A diagnosis of psoriasis is usually based on the appearance of the skin. Skin characteristics typical for psoriasis are scaly,
erythematous plaques, papules, or patches of skin that may be painful and itch. No special blood tests or diagnostic
procedures are usually required to make the diagnosis.
The differential diagnosis of psoriasis includes dermatological conditions similar in appearance such as discoid eczema,
seborrhoeic eczema, pityriasis rosea (may be confused with guttate psoriasis), nail fungus (may be confused with nail psoriasis)
or cutaneous T cell lymphoma (50% of individuals with this cancer are initially misdiagnosed with psoriasis). Dermatologic
manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis.

If the clinical diagnosis is uncertain, a skin biopsy or scraping may be performed to rule out other disorders and to confirm
the diagnosis. Skin from a biopsy will show clubbed epidermal projections that interdigitate with dermis on microscopy.
Epidermal thickening is another characteristic histologic finding of psoriasis lesions. The stratum granulosum layer of the
epidermis is often missing or significantly decreased in psoriatic lesions; the skin cells from the most superficial layer of skin
are also abnormal as they never fully mature. Unlike their mature counterparts, these superficial cells keep their nucleus.
Inflammatory infiltrates can typically be visualized on microscopy when examining skin tissue or joint tissue affected by
psoriasis. Epidermal skin tissue affected by psoriatic inflammation often has many CD8+ T cells while a predominance of
CD4+ T cells makes up the inflammatory infiltrates of the dermal layer of skin and the joints.
MANAGEMENT
While no cure is available for psoriasis, many treatment options exist. Topical agents are typically used for mild disease,
phototherapy for moderate disease, and systemic agents for severe disease.
TOPICAL AGENTS
Topical corticosteroid preparations are the most effective agents when used continuously for 8 weeks; retinoids and coal tar
were found to be of limited benefit and may be no better than placebo. Greater benefit has been observed with very potent
corticosteroids when compared to potent corticosteroids.
Vitamin D analogues such as paricalcitol were found to be superior to placebo. Combination therapy with vitamin D and a
corticosteroid was superior to either treatment alone and vitamin D was found to be superior to coal tar for chronic plaque
psoriasis.
Moisturizers and emollients such as mineral oil, petroleum jelly, calcipotriol, and decubal (an oil-in-water emollient) were
found to increase the clearance of psoriatic plaques. Emollients have been shown to be even more effective at clearing
psoriatic plaques when combined with phototherapy. However, certain emollients have no impact on psoriasis plaque
clearance or may even decrease the clearance achieved with phototherapy. The emollient salicylic acid is structurally similar
to para-aminobenzoic acid (PABA), commonly found in sunscreen, and is known to interfere with phototherapy in psoriasis.
Coconut oil, when used as an emollient in psoriasis, has been found to decrease plaque clearance with phototherapy.
Medicated creams and ointments applied directly to psoriatic plaques can help reduce inflammation, remove built-up scale,
reduce skin turnover, and clear affected skin of plaques. Ointment and creams containing coal tar, dithranol, corticosteroids
(i.e. desoximetasone), fluocinonide, vitamin D3 analogs (for example, calcipotriol), and retinoids are routinely used. The use
of the finger tip unit may be helpful in guiding how much topical treatment to use.
Vitamin D analogues may be useful with steroids; however, alone have a higher rate of side effects. They may allow less
steroids to be used.
UV PHOTOTHERAPY
Phototherapy in the form of sunlight has long been used for psoriasis. UVB Wavelengths of 311–313 nanometers are most
effective, and special lamps have been developed for this application. The exposure time should be controlled to avoid over

exposure and burning of the skin. The UVB lamps should have a timer that will turn off the lamp when the time ends. The
amount of light used is determined by a person's skin type. Increased rates of cancer from treatment appear to be small.
Narrow band UVB light (NBUVB) phototherapy has been demonstrated to have similar efficacy to Psoralen and ultraviolet A
phototherapy (PUVA).
SYSTEMIC AGENTS
Psoriasis resistant to topical treatment and phototherapy may be treated with systemic therapies including medications by
mouth or injectable treatments. People undergoing systemic treatment must have regular blood and liver function tests to
check for medication toxicities. Pregnancy must be avoided for most of these treatments. The majority of people experience
a recurrence of psoriasis after systemic treatment is discontinued.
Non-biologic systemic treatments frequently used for psoriasis include methotrexate, ciclosporin, hydroxycarbamide,
fumarates such as dimethyl fumarate, and retinoids. Methotrexate and ciclosporin are drugs that suppress the immune
system; retinoids are synthetic forms of vitamin A. These agents are also regarded as first-line treatments for psoriatic
erythroderma. Oral corticosteroids should not be used, for they can severely flare psoriasis upon their discontinuation.
SURGERY
Limited evidence suggests removal of the tonsils may benefit people with chronic plaque psoriasis, guttate psoriasis, and
palmoplantar pustulosis.
DIET
Uncontrolled studies have suggested that individuals with psoriasis or psoriatic arthritis may benefit from a diet supplemented
with fish oil rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Diet recommendations include consumption
of cold water fish (preferably wild fish, not farmed) such as salmon, herring, and mackerel; extra virgin olive oil; legumes;
vegetables; fruits; and whole grains; and avoid consumption of alcohol, red meat, and dairy products. The effect of
consumption of caffeine (including coffee, black tea, mate, and dark chocolate) remains to be determined.
There is a higher rate of celiac disease among people with psoriasis. When adopting a gluten-free diet, disease severity
generally decreases in people with celiac disease and those with anti-gliadin antibodies.

11. ERYTHRODERMA
Erythroderma (also known as "Exfoliative dermatitis," "Dermatitis exfoliativa") is an inflammatory skin disease with erythema
and scaling that affects nearly the entire cutaneous surface.
Erythroderma is generalized exfoliative dermatitis, which involves 90% or more of the patient's skin. The most common cause
of erythroderma is exacerbation of an underlying skin disease, such as psoriasis, contact dermatitis, seborrheic dermatitis,
lichen planus, pityriasis rubra pilaris or a drug reaction. Primary erythroderma is less frequent and is usually seen in cases of
cutaneous T-cell lymphoma, in particular in Sézary's disease.
The most common causes of exfoliative dermatitis are best remembered by the mnemonic device ID-SCALP. The causes and
their frequencies are as follows:
 Idiopathic - 30%
 Drug allergy - 28%
 Lymphoma and leukemia - 14%
 Atopic dermatitis - 10%
 Psoriasis - 8%
 Contact dermatitis - 3%
 Seborrheic dermatitis - 2%
Differential diagnosis in patients with erythroderma may be difficult.
TREATMENT
The primary cause has to be treated, or the exacerbation may persisist and reincide. Topical steroids are the primary category
of medications used to treat exfoliative dermatitis (ED). A sedative antihistamine may be a useful adjunct for pruritic patients,
since it helps patients to sleep at night, thus limiting nocturnal scratching and excoriations. Antimicrobial agents often are
used if an infection is suspected to be precipitating or complicating exfoliative dermatitis. Other drugs specifically indicated
for management of underlying cause of exfoliative dermatitis may be necessary.
PREVENTIVE AND PROMOTIVE OF SKIN HEALTH MEASURES.

 Seek the shade, especially between 10 AM and 4 PM.
 Do not burn.
 Avoid tanning and UV tanning beds.
 Cover up with clothing, including a broad-brimmed hat and UV-blocking sunglasses.
 Use a broad spectrum (UVA/UVB) sunscreen with an SPF of 15 or higher every day. For extended outdoor activity,
use a water-resistant, broad spectrum (UVA/UVB) sunscreen with an SPF of 30 or higher.
 Apply 1 ounce (2 tablespoons) of sunscreen to your entire body 30 minutes before going outside.Reapply every two
hours or immediately after swimming or excessive sweating.

 Keep newborns out of the sun. Sunscreens should be used on babies over the age of six months.
 Examine your skin head-to-toe every month.
 See your physician every year for a professional skin exam.

SEXUALLY TRANSMITTED INFECTIONS
1. BACTERIAL
I. GONORRHEA
Gonorrhea, also spelled gonorrhea, is a sexually transmitted infection (STI) caused by the bacterium Neisseria gonorrhoeae.
SIGNS AND SYMPTOMS

Half of women with gonorrhea do not have symptoms, whereas others have vaginal discharge, lower abdominal pain, or pain
with sexual intercourse associated with inflammation of the uterine cervix. Most infected men with symptoms have
inflammation of the penile urethra associated with a burning sensation during urination and discharge from the penis. In
men, discharge with or without burning occurs in half of all cases and is the most common symptom of the infection. Men
and women can acquire gonorrhea of the throat from performing oral sex on an infected partner, usually a male partner.
Such infection does not produce symptoms in 90% of cases and produces a sore throat in the remaining 10%. In advanced
cases, gonorrhea may cause a general feeling of tiredness similar to other infections. It is also possible for an individual to
have an allergic reaction to the bacteria, in which case any appearing symptoms will be greatly intensified.
The incubation period is 2 to 14 days, with most symptoms appearing between 4 and 6 days after infection. Rarely, gonorrhea
may cause skin lesions and joint infection (pain and swelling in the joints) after traveling through the blood stream (see below).
Very rarely it may settle in the heart causing endocarditis or in the spinal column causing meningitis (both are more likely
among individuals with suppressed immune systems, however).
Having a case of gonorrhea is associated with an increased risk of developing prostate cancer.
SPREAD
The infection is usually spread from one person to another through vaginal, oral, or anal sex. Men have a 20% risk of getting
the infection from a single act of vaginal intercourse with an infected woman. The risk for men that have sex with men (MSM)
is higher. Active MSM may get a penile infection, while passive MSM may get anorectal gonorrhea. Women have a 60–80%
risk of getting the infection from a single act of vaginal intercourse with an infected man. A pregnant woman can pass on the
infection to her unborn infant.
A mother may transmit gonorrhea to her newborn during childbirth; when affecting the infant's eyes, it is referred to as
ophthalmia neonatorum. It may be able to spread through the objects contaminated with body fluid from an infected person.
The bacteria typically does not survive long outside the body, typically dying within minutes to hours.
DIAGNOSIS
Traditionally, gonorrhea was diagnosed with gram stain and culture; however, newer polymerase chain reaction (PCR)-based
testing methods are becoming more common. In those failing initial treatment, culture should be done to determine
sensitivity to antibiotics.

Tests that use polymerase chain reaction (PCR, aka nucleic acid amplification) to identify genes unique to N. gonorrhoeae
are recommended for screening and diagnosis of gonorrhea infection. These PCR-based tests require a sample of urine,
urethral swabs, or cervical/vaginal swabs. Culture (growing colonies of bacteria in order to isolate and identify them) and
gram-stain (staining of bacterial cell walls to reveal morphology) can also be used to detect the presence of N. gonorrhoeae
in all specimen types except urine.
TREATMENT
As of 2010, injectable ceftriaxone is one of the few effective antibiotics. This is typically given in combination with either
azithromycin or doxycycline. As of 2015 and 2016 the CDC and WHO only recommends both ceftriaxone and azithromycin.
Because of increasing rates of antibiotic resistance local susceptibility patterns must be taken into account when deciding on
treatment.
PROGNOSIS
Gonorrhea if left untreated may last for weeks or months with higher risks of complications. One of the complications of
gonorrhea is systemic dissemination resulting in skin pustules or petechia, septic arthritis, meningitis, or endocarditis. This
occurs in between 0.6 and 3% of infected women and 0.4 and 0.7% of infected men.
In men, inflammation of the epididymis, prostate gland, and urethra can result from untreated gonorrhea. In women, the
most common result of untreated gonorrhea is pelvic inflammatory disease. Other complications include inflammation of the
tissue surrounding the liver, a rare complication associated with Fitz-Hugh–Curtis syndrome; septic arthritis in the fingers,
wrists, toes, and ankles; septic abortion; chorioamnionitis during pregnancy; neonatal or adult blindness from conjunctivitis;
and infertility. Men who have had a gonorrhea infection have an increased risk of getting prostate cancer.
Newborn babies coming through the birth canal are given erythromycin ointment in the eyes to prevent blindness from
infection. The underlying gonorrhea should be treated; if this is done then usually a good prognosis will follow. Adults may
also have eyes infected with gonorrhoea and require proper personal hygiene and medications.
Among persons in the United States between 14 and 39 years of age, 46% of people with gonorrheal infection also have
chlamydial infection.
II. SYPHILIS
Syphilis is a sexually transmitted infection caused by the bacterium Treponema pallidum subspecies pallidum.
SIGNS AND SYMPTOMS

Primary syphilis is typically acquired by direct sexual contact with the infectious lesions of another person. Approximately 3
to 90 days after the initial exposure (average 21 days) a skin lesion, called a chancre, appears at the point of contact. This is
classically (40% of the time) a single, firm, painless, non-itchy skin ulceration with a clean base and sharp borders 0.3–3.0 cm
in size. The lesion may take on almost any form. In the classic form, it evolves from a macule to a papule and finally to an
erosion or ulcer. Occasionally, multiple lesions may be present (~40%), with multiple lesions more common when coinfected
with HIV. Lesions may be painful or tender (30%), and they may occur in places other than the genitals (2–7%). The most
common location in women is the cervix (44%), the penis in heterosexual men (99%), and anally and rectally relatively
commonly in men who have sex with men (34%). Lymph node enlargement frequently (80%) occurs around the area of
infection, occurring seven to 10 days after chancre formation. The lesion may persist for three to six weeks without treatment.
Secondary syphilis occurs approximately four to ten weeks after the primary infection. While secondary disease is known for
the many different ways it can manifest, symptoms most commonly involve the skin, mucous membranes, and lymph nodes.
There may be a symmetrical, reddish-pink, non-itchy rash on the trunk and extremities, including the palms and soles. The
rash may become maculopapular or pustular. It may form flat, broad, whitish, wart-like lesions known as condyloma latum
on mucous membranes. All of these lesions harbor bacteria and are infectious. Other symptoms may include fever, sore
throat, malaise, weight loss, hair loss, and headache. Rare manifestations include liver inflammation, kidney disease, joint
inflammation, periostitis, inflammation of the optic nerve, uveitis, and interstitial keratitis. The acute symptoms usually resolve
after three to six weeks; about 25% of people may present with a recurrence of secondary symptoms. Many people who
present with secondary syphilis (40–85% of women, 20–65% of men) do not report previously having had the classic chancre
of primary syphilis.
Latent syphilis is defined as having serologic proof of infection without symptoms of disease. It is further described as either
early (less than 1 year after secondary syphilis) or late (more than 1 year after secondary syphilis) in the United States. The
United Kingdom uses a cut-off of two years for early and late latent syphilis. Early latent syphilis may have a relapse of
symptoms. Late latent syphilis is asymptomatic, and not as contagious as early latent syphilis.
Tertiary syphilis may occur approximately 3 to 15 years after the initial infection, and may be divided into three different forms:
gummatous syphilis (15%), late neurosyphilis (6.5%), and cardiovascular syphilis (10%). Without treatment, a third of infected
people develop tertiary disease. People with tertiary syphilis are not infectious. Gummatous syphilis or late benign syphilis
usually occurs 1 to 46 years after the initial infection, with an average of 15 years. This stage is characterized by the formation
of chronic gummas, which are soft, tumor-like balls of inflammation which may vary considerably in size. They typically affect
the skin, bone, and liver, but can occur anywhere. Neurosyphilis refers to an infection involving the central nervous system. It
may occur early, being either asymptomatic or in the form of syphilitic meningitis, or late as meningovascular syphilis, general
paresis, or tabes dorsalis, which is associated with poor balance and lightning pains in the lower extremities. Late neurosyphilis
typically occurs 4 to 25 years after the initial infection. Meningovascular syphilis typically presents with apathy and seizure,
and general paresis with dementia and tabes dorsalis. Also, there may be Argyll Robertson pupils, which are bilateral small
pupils that constrict when the person focuses on near objects but do not constrict when exposed to bright light.
Cardiovascular syphilis usually occurs 10–30 years after the initial infection. The most common complication is syphilitic aortitis,
which may result in aneurysm formation.
TRANSMISSION
Syphilis is transmitted primarily by sexual contact or during pregnancy from a mother to her fetus; the spirochete is able to
pass through intact mucous membranes or compromised skin. It is thus transmissible by kissing near a lesion, as well as oral,

vaginal, and anal sex. Approximately 30% to 60% of those exposed to primary or secondary syphilis will get the disease. Its
infectivity is exemplified by the fact that an individual inoculated with only 57 organisms has a 50% chance of being infected.
Most (60%) of new cases in the United States occur in men who have sex with men. Syphilis can be transmitted by blood
products, but the risk is low due to blood testing in many countries. The risk of transmission from sharing needles appears
limited.
It is not generally possible to contract syphilis through toilet seats, daily activities, hot tubs, or sharing eating utensils or
clothing. This is mainly because the bacteria die very quickly outside of the body, making transmission by objects extremely
difficult.
DIAGNOSIS
Syphilis is difficult to diagnose clinically early in its presentation. Confirmation is either via blood tests or direct visual inspection
using microscopy. Blood tests are more commonly used, as they are easier to perform. Diagnostic tests are unable to
distinguish between the stages of the disease.
Blood tests
Blood tests are divided into nontreponemal and treponemal tests.
Nontreponemal tests are used initially and include venereal disease research laboratory (VDRL) and rapid plasma reagin (RPR)
tests. False positives on the nontreponemal tests can occur with some viral infections, such as varicella (chickenpox) and
measles. False positives can also occur with lymphoma, tuberculosis, malaria, endocarditis, connective tissue disease, and
pregnancy.
Because of the possibility of false positives with nontreponemal tests, confirmation is required with a treponemal test, such
as treponemal pallidum particle agglutination (TPHA) or fluorescent treponemal antibody absorption test (FTA-Abs).
Treponemal antibody tests usually become positive two to five weeks after the initial infection. Neurosyphilis is diagnosed by
finding high numbers of leukocytes (predominately lymphocytes) and high protein levels in the cerebrospinal fluid in the
setting of a known syphilis infection.
Direct testing
Dark ground microscopy of serous fluid from a chancre may be used to make an immediate diagnosis. Hospitals do not
always have equipment or experienced staff members, and testing must be done within 10 minutes of acquiring the sample.
Sensitivity has been reported to be nearly 80%; therefore the test can only be used to confirm a diagnosis, but not to rule
one out.
TREATMENT
Early infections
The first-choice treatment for uncomplicated syphilis remains a single dose of intramuscular benzathine benzylpenicillin.
Doxycycline and tetracycline are alternative choices for those allergic to penicillin; due to the risk of birth defects, these are
not recommended for pregnant women. Resistance to macrolides, rifampicin, and clindamycin is often present. Ceftriaxone,
a third-generation cephalosporin antibiotic, may be as effective as penicillin-based treatment. It is recommended that a
treated person avoid sex until the sores are healed.

Late infections
For neurosyphilis, due to the poor penetration of benzylpenicillin into the central nervous system, those affected are
recommended to be given large doses of intravenous penicillin for a minimum of 10 days. If a person is allergic, ceftriaxone
may be used or penicillin desensitization attempted. Other late presentations may be treated with once-weekly intramuscular
benzylpenicillin for three weeks. If allergic, as in the case of early disease, doxycycline or tetracycline may be used, albeit for
a longer duration. Treatment at this stage limits further progression but has only slight effect on damage which has already
occurred.
Jarisch-Herxheimer reaction
One of the potential side effects of treatment is the Jarisch-Herxheimer reaction. It frequently starts within one hour and lasts
for 24 hours, with symptoms of fever, muscle pains, headache, and a fast heart rate. It is caused by cytokines released by the
immune system in response to lipoproteins released from rupturing syphilis bacteria.
Pregnancy
Penicillin is an effective treatment for syphilis in pregnancy but there is no agreement on which dose or way of giving it is
most effective. More research is needed into how much antibiotic to give and when to give it.
III. CHLAMYDIA
Chlamydia infection, often simply known as chlamydia, is a sexually transmitted infection caused by the bacterium Chlamydia
trachomatis. Most people who are infected have no symptoms. When symptoms do develop this can take a few weeks
following infection to occur. Symptoms in women may include vaginal discharge or burning with urination. Symptoms in men
may include discharge from the penis, burning with urination, or pain and swelling of one or both testicles. The infection can
spread to the upper genital tract in women causing pelvic inflammatory disease which may result in future infertility or ectopic
pregnancy. Repeated infections of the eyes that go without treatment can result in trachoma, a common cause of blindness
in the developing world.
Chlamydia can be spread during vaginal, anal, or oral sex, and can be passed from an infected mother to her baby during
childbirth. The eye infections may also be spread by personal contact, flies, and contaminated towels in areas with poor
sanitation. Chlamydia trachomatis only occurs in humans. Diagnosis is often by screening which is recommended yearly in
sexually active women under the age of twenty five, others at higher risk, and at the first prenatal visit. Testing can be done
on the urine or a swab of the cervix, vagina, or urethra. Rectal or mouth swabs are required to diagnose infections in those
areas.
Prevention is by not having sex, the use of condoms, or having sex with only one other person, who is not infected. Chlamydia
can be cured by antibiotics with typically either azithromycin or doxycycline being used. Erythromycin or azithromycin is
recommended in babies and during pregnancy. Sexual partners should also be treated and the infected people advised not

to have sex for seven days and until symptom free. Gonorrhea, syphilis, and HIV should be tested for in those who have been
infected. Following treatment people should be tested again after three months.
Chlamydia is one of the most common sexually transmitted infections worldwide affecting about 4.2% of women and 2.7%
of men. In 2015 about 61 million new cases occurred globally. In the United States about 1.4 million cases were reported in
2014. Infections are most common among those between the ages of 15 and 25 and are more common in women than men.
In 2015 infections resulted in about 200 deaths. The word "chlamydia" is from the Greek, χλαμύδα meaning "cloak".
LYMPHOGRANULOMA VENERUM
It is a sexually transmitted disease caused by the invasive serovars L1, L2, L2a or L3 of Chlamydia trachomatis.
SIGNS AND SYMPTOMS

The clinical manifestation of LGV depends on the site of entry of the infectious organism (the sex contact site) and the stage
of disease progression.
 Inoculation at the mucous lining of external sex organs (penis and vagina) can lead to the inguinal syndrome named
after the formation of buboes or abscesses in the groin (inguinal) region where draining lymph nodes are located.
These signs usually appear from 3 days to a month after exposure.
 The rectal syndrome (Lymphogranuloma venereum proctitis, or LGVP) arises if the infection takes place via the rectal
mucosa (through anal sex) and is mainly characterized by proctocolitis or proctitis symptoms.
 The pharyngeal syndrome is rare. It starts after infection of pharyngeal tissue, and buboes in the neck region can
occur.
Primary stage
LGV may begin as a self-limited painless genital ulcer that occurs at the contact site 3–12 days after infection. Women rarely
notice a primary infection because the initial ulceration where the organism penetrates the mucosal layer is often located out
of sight, in the vaginal wall. In men fewer than 1/3 of those infected notice the first signs of LGV. This primary stage heals in
a few days. Erythema nodosum occurs in 10% of cases.
Secondary stage
The secondary stage most often occurs 10–30 days later, but can present up to six months later. The infection spreads to the
lymph nodes through lymphatic drainage pathways. The most frequent presenting clinical manifestation of LGV among males
whose primary exposure was genital is unilateral (in 2/3 of cases) lymphadenitis and lymphangitis, often with tender inguinal
and/or femoral lymphadenopathy because of the drainage pathway for their likely infected areas. Lymphangitis of the dorsal
penis may also occur and resembles a string or cord. If the route was anal sex the infected person may experience
lymphadenitis and lymphangitis noted above. They may instead develop proctitis, inflammation limited to the rectum (the
distal 10–12 cm) that may be associated with anorectal pain, tenesmus, and rectal discharge, or proctocolitis, inflammation of
the colonic mucosa extending to 12 cm above the anus and associated with symptoms of proctitis plus diarrhea or abdominal
cramps.

In addition, symptoms may include inflammatory involvement of the perirectal or perianal lymphatic tissues. In females,
cervicitis, perimetritis, or salpingitis may occur as well as lymphangitis and lymphadenitis in deeper nodes. Because of
lymphatic drainage pathways, some patients develop an abdominal mass which seldom suppurates, and 20–30% develop
inguinal lymphadenopathy. Systemic signs which can appear include fever, decreased appetite, and malaise. Diagnosis is
more difficult in women and men who have sex with men (MSM) who may not have the inguinal symptoms.
Over the course of the disease, lymph nodes enlarge, as may occur in any infection of the same areas as well. Enlarged nodes
are called buboes. Buboes are commonly painful. Nodes commonly become inflamed, thinning and fixation of the overlying
skin. These changes may progress to necrosis, fluctuant and suppurative lymph nodes, abscesses, fistulas, strictures, and sinus
tracts. During the infection and when it subsides and healing takes place, fibrosis may occur. This can result in varying degrees
of lymphatic obstruction, chronic edema, and strictures. These late stages characterised by fibrosis and edema are also known
as the third stage of LGV and are mainly permanent.
DIAGNOSIS
The diagnosis usually is made serologically (through complement fixation) and by exclusion of other causes of inguinal
lymphadenopathy or genital ulcers. Serologic testing has a sensitivity of 80% after 2 weeks. Serologic testing may not be
specific for serotype (has some cross reactivity with other chlamydia species) and can suggest LGV from other forms because
of their difference in dilution, 1:64 more likely to be LGV and lower than 1:16 is likely to be other chlamydia forms.
For identification of serotypes, culture is often used . Culture is difficult. Requiring a special medium, cycloheximide-treated
McCoy or HeLa cells, and yields are still only 30-50%. DFA, or direct fluorescent antibody test, PCR of likely infected areas
and pus, are also sometimes used. DFA test for the L-type serovar of C trachomatis is the most sensitive and specific test, but
is not readily available.
If polymerase chain reaction (PCR) tests on infected material are positive, subsequent restriction endonuclease pattern
analysis of the amplified outer membrane protein A gene can be done to determine the genotype.
Recently a fast realtime PCR (TaqMan analysis) has been developed to diagnose LGV. With this method an accurate diagnosis
is feasible within a day. It has been noted that one type of testing may not be thorough enough.
TREATMENT
Treatment involves antibiotics and may involve drainage of the buboes or abscesses by needle aspiration or incision. Further
supportive measure may need to be taken: dilatation of the rectal stricture, repair of rectovaginal fistulae, or colostomy for
rectal obstruction.
Common antibiotic treatments include: tetracycline (doxycycline) (all tetracyclines, including doxycycline, are contraindicated
during pregnancy and in children due to effects on bone development and tooth discoloration), and erythromycin.
Azithromycin is also a drug of choice in LGV.
PROGNOSIS

Prognosis is highly variable. Spontaneous remission is common. Complete cure can be obtained with proper antibiotic
treatments to kill the causative bacteria, such as tetracycline, doxycycline, or erythromycin. Prognosis is more favorable with
early treatment. Bacterial superinfections may complicate course. Death can occur from bowel obstruction or perforation,
and follicular conjunctivitis due to autoinoculation of infectious discharge can occur.
LONG TERM COMPLICATIONS

Genital elephantiasis or esthiomene, which is the dramatic end-result of lymphatic obstruction, which may occur because of
the strictures themselves, or fistulas. This is usually seen in females, may ulcerate and often occurs 1–20 years after primary
infection. Fistulas of, but not limited to, the penis, urethra, vagina, uterus, or rectum. Also, surrounding edema often occurs.
Rectal or other strictures and scarring. Systemic spread may occur, possible results are arthritis, pneumonitis, hepatitis, or
perihepatitis.
IV. CHANCROID
Chancroid is a bacterial infection caused by the fastidious Gram-negative streptobacillus Haemophilus ducreyi. It is a disease
found primarily in developing countries, most prevalent in low socioeconomic groups, associated with commercial sex
workers. Chancroid is a risk factor for contracting HIV, due to their ecological association or shared risk of exposure, and
biologically facilitated transmission of one infection by the other. Approximately 10% of people with chacroid will have a co-
infection with syphilis and/or HIV. H. ducreyi enters skin through microabrasions incurred during sexual intercourse. A local
tissue reaction leads to development of erythomatous papule, which progresses to pustule in 4–7 days. It then undergoes
central necrosis to ulcerate.
SIGNS AND SYMPTOMS

These are only local and no systemic manifestations are present. The ulcer characteristically:
 Ranges in size dramatically from 3 to 50 mm (1/8 inch to two inches) across
 Is painful
 Has sharply defined, undermined borders
 Has irregular or ragged borders
 Has a base that is covered with a gray or yellowish-gray material
 Has a base that bleeds easily if traumatized or scraped
 painful swollen lymph nodes occurs in 30 to 60% of patients.
 dysuria (pain with urination) and dyspareunia (pain with intercourse) in females
About half of infected men have only a single ulcer. Women frequently have four or more ulcers, with fewer symptoms.
The initial ulcer may be mistaken as a "hard" chancre, the typical sore of primary syphilis, as opposed to the "soft chancre" of
chancroid.
Approximately one-third of the infected individuals will develop enlargements of the inguinal lymph nodes, the nodes located
in the fold between the leg and the lower abdomen.
Half of those who develop swelling of the inguinal lymph nodes will progress to a point where the nodes rupture through
the skin, producing draining abscesses. The swollen lymph nodes and abscesses are often referred to as buboes.
Males  Coronal sulcus

 Internal and external surface of prepuce.  Frenulum

 Shaft of penis
 Prepucial orifice
 Urethral meatus
 Glans penis
 Perineum area
Females
 Labia majora is most common site. "Kissing ulcers"
may develop. These are ulcers that occur on
opposing surfaces of the labia.
 Labia minora
 Fourchette
 Vestibule
 Clitoris
 Perineal area
 Inner thighs

DIAGNOSIS
Variants
Some of clinical variants are as follows.
VARIANT CHARACTERISTICS
Transient Superficial ulcers that may heal rapidly, followed by a typical inguinal bubo.
chancroid
Serpiginous Multiple ulcers that coalesce to form a serpiginous pattern.

chancroid
Phagedenic Ulceration that causes extensive destruction of genitalia following secondary or superinfection by
chancroid anaerobes such as Fusobacterium or Bacteroides.
Mixed chancroid Nonindurated tender ulcers of chancroid appearing together with an indurated nontender ulcer of
syphilis having an incubation period of 10 to 90 days.
Giant chancroid Large granulomatous ulcer at the site of a ruptured inguinal bubo, extending beyond its margins.
Follicular Seen in females in association with hair follicles of the labia majora and pubis; initial follicular pustule
chancroid evolves into a classic ulcer at the site.
Dwarf chancroid Small, superficial, relatively painless ulcer.
Chancroidal ulcer Most often a tender, nonindurated, single large ulcer caused by organisms other than Haemophilus
ducreyi; lymphadenopathy is conspicuous by its absence.
Laboratory findings
From bubo pus or ulcer secretions, H. ducreyi can be identified. PCR-based identification of organisms is available. Simple,
rapid, sensitive and inexpensive antigen detection methods for H. ducreyi identification are also popular. Serologic detection
of H. ducreyi is and uses outer membrane protein and lipooligosaccharide.
CDC's standard clinical definition for a probable case of chancroid

Patient has one or more painful genital ulcers. The combination of a painful ulcer with tender adenopathy is suggestive of
chancroid; the presence of suppurative adenopathy is almost pathognomonic.
 No evidence of Treponema pallidum infection by darkfield microscopic examination of ulcer exudate or by a serologic
test for syphilis performed greater than or equal to 7 days after onset of ulcers and
 Either a clinical presentation of the ulcer(s) not typical of disease caused by herpes simplex virus (HSV) or a culture
negative for HSV.
MISS ANNE ODARO | DERMATOVENEOROLOGY

Despite many distinguishing features, the clinical spectrums of following diseases may overlap with chancroid:
 Primary syphilis
 Genital herpes
Practical clinical approach for this STI as Genital Ulcer Disease is to rule out top differential diagnosis of Syphilis and Herpes
and consider empirical treatment for Chancroid as testing is not commonly done for the latter.
Comparison with syphilis

There are many differences and similarities between the conditions syphilitic chancre and chancroid.
Similarities
 Both originate as pustules at the site of inoculation, and progress to ulcerated lesions
 Both lesions are typically 1–2 cm in diameter
 Both lesions are caused by sexually transmissible organisms
 Both lesions typically appear on the genitals of infected individuals
 Both lesions can be present at multiple sites and with multiple lesions
Differences
 Chancre is a lesion typical of infection with the bacterium that causes syphilis, Treponema pallidum
 Chancroid is a lesion typical of infection with the bacterium Haemophilus ducreyi
 Chancres are typically painless, whereas chancroid are typically painful
 Chancres are typically non-exudative, whereas chancroid typically have a grey or yellow purulent exudate
 Chancres have a hard (indurated) edge, whereas chancroid have a soft edge
 Chancres heal spontaneously within three to six weeks, even in the absence of treatment
 Chancres can occur in the pharynx as well as on the genitals
TREATMENT
 The CDC recommendation for chancroid is a single oral dose (1 gram) of azithromycin, or a single IM dose of ceftriaxone,
or oral erythromycin for seven days.
 Abscesses are drained.
 H. ducreyi is resistant to sulfonamides, tetracyclines, penicillins, chloramphenicol, ciprofloxacin, ofloxacin, trimethoprim
and aminoglycosides. Recently, several erythromycin resistant isolates have been reported.
 Treatment failure is possible with HIV co-infection and extended therapy is sometimes required.
COMPLICATIONS
 Extensive adenitis may develop.
 Large inguinal abscesses may develop and rupture to form draining sinus or giant ulcer.
 Superinfection by Fusarium and Bacteroides. These later require debridement and may result in disfiguring scars.
 Phimosis can develop in long standing lesion by scarring and thickening of foreskin, which may subsequently require
circumcision.

V. GRANULOMA INGUINALE
Granuloma inguinale (also known as donovanosis) is a bacterial disease caused by Klebsiella granulomatis (formerly known
as Calymmatobacterium granulomatis) characterized by genital ulcers. It is endemic in many less developed regions. It is also
known as donovanosis, granuloma genitoinguinale, granuloma inguinale tropicum, granuloma venereum, granuloma
venereum genitoinguinale, lupoid form of groin ulceration, serpiginous ulceration of the groin, ulcerating granuloma of the
pudendum, and ulcerating sclerosing granuloma.
SYMPTOMS
Small, painless nodules appear after about 10–40 days of the contact with the bacteria. Later, the nodules burst, creating
open, fleshy, oozing lesions. The infection spreads, mutilating the infected tissue. The infection will continue to destroy the
tissue until treated. The lesions occur at the region of contact typically found on the shaft of the penis, the labia, or the
perineum. Rarely, the vaginal wall or cervix is the site of the lesion. At least one case in India led to partial autoamputation of
the penis. The patient tested positive for HIV-2 and had been infected for six years.
The microorganism spreads from one host to another through contact with the open sores.
DIAGNOSIS
The diagnosis is based on the patient's sexual history and on physical examination revealing a painless, "beefy-red ulcer" with
a characteristic rolled edge of granulation tissue. In contrast to syphilitic ulcers, inguinal lymphadenopathy is generally mild
or absent. Tissue biopsy and Wright-Giemsa stain are used to aid in the diagnosis. The presence of Donovan bodies in the
tissue sample confirms donovanosis. Donovan bodies are rod-shaped, oval organisms that can be seen in the cytoplasm of
mononuclear phagocytes or histiocytes in tissue samples from patients with granuloma inguinale.
They appear deep purple when stained with Wright's stain. These intracellular inclusions are the encapsulated Gram-negative
rods of the causative organisms.[6] They were discovered by Charles Donovan.
TREATMENT
Recommended regimen is:
 azithromycin 100 mg orally twice a day, alternatively
 doxycycline 1 g orally once per week or
 ciprofloxacin 750 mg orally twice a day or
 erythromycin base 500 mg orally four times a day or
 trimethoprim-sulfamethoxazole one double-strength (160 mg/800 mg) tablet orally twice a day.

All antibiotic regimens should last for at least 3 weeks and until all lesions have completely healed. Normally, the infection
will begin to subside within a week of treatment, but the full treatment period must be followed to minimize the possibility
of relapse.
According to the CDC 2015 guidelines Azithromycin is the antibiotic of choice.

2. PARASITIC
I. TRICHOMONAS VAGINALIS
Trichomonas vaginalis is an anaerobic, flagellated protozoan parasite and the causative agent of trichomoniasis. It is the most
common pathogenic protozoan infection of humans in industrialized countries. Infection rates between men and women are
similar with women being symptomatic, while infections in men are usually asymptomatic.
Trichomonas vaginalis, a parasitic protozoan, is the etiologic agent of trichomoniasis, and is a sexually transmitted infection.
More than 160 million people worldwide are annually infected by this protozoan.
SYMPTOMS
Trichomoniasis, a sexually transmitted infection of the urogenital tract, is a common cause of vaginitis in women, while men
with this infection can display symptoms of urethritis. 'Frothy', greenish vaginal discharge with a 'musty' malodorous smell is
characteristic.
SIGNS
Only 2% of women with the infection will have a "strawberry" cervix (colpitis macularis, an erythematous cervix with pinpoint
areas of exudation) or vagina on examination. This is due to capillary dilation as a result of the inflammatory response.
COMPLICATIONS
Some of the complications of T. vaginalis in women include: preterm delivery, low birth weight, and increased mortality as
well as predisposing to HIV infection, AIDS, and cervical cancer. T. vaginalis has also been reported in the urinary tract,
fallopian tubes, and pelvis and can cause pneumonia, bronchitis, and oral lesions. Condoms are effective at reducing, but not
wholly preventing, transmission.
Trichomonas vaginalis infection in males has been found to cause asymptomatic urethritis and prostatitis. It has been
proposed that it may increase the risk of prostate cancer; however, evidence is insufficient to support this association as of
2014.
DIAGNOSIS
Classically, with a cervical smear, infected women have a transparent "halo" around their superficial cell nucleus. It is unreliably
detected by studying a genital discharge or with a cervical smear because of their low sensitivity. T. vaginalis was traditionally
diagnosed via a wet mount, in which "corkscrew" motility was observed. Currently, the most common method of diagnosis is
via overnight culture, with a sensitivity range of 75–95%. Newer methods, such as rapid antigen testing and transcription-
mediated amplification, have even greater sensitivity, but are not in widespread use. The presence of T. vaginalis can also be
diagnosed by PCR, using primers specific for GENBANK/L23861.
TREATMENT

Infection is treated and cured with metronidazole or tinidazole. The CDC recommends a one time dose of 2 grams of either
metronidazole or tinidazole as the first-line treatment; the alternate treatment recommended is 500 milligrams of
metronidazole, twice daily, for seven days if there is failure of the single-dose regimen. Medication should be prescribed to
any sexual partner(s) as well because they may be asymptomatic carriers.
II. PTHIRUS PUBIS

The crab louse or pubic louse (Pthirus pubis) is an insect that is an obligate ectoparasite of humans, feeding exclusively on
blood. The crab louse usually is found in the person's pubic hair. Although the louse cannot jump, it can also live in other
areas of the body that are covered with coarse hair, such as the eyelashes. It is of the order Psocodea.
Humans are the only known hosts of the crab louse, although a closely related species, Pthirus gorillae, infects gorilla
populations. The human parasite diverged from Pthirus gorillae approximately 3.3 million years ago. It is more distantly
related to the genus Pediculus, which contains the human head and body lice and a louse that affects chimpanzees and
bonobos.
INFESTATION IN HUMANS
nfestations of crab lice are known as pediculosis pubis or phthiriasis pubis (which, unlike the generic name of the louse, is
spelled with a phth). Infestation of the eyelashes is referred to as pediculosis ciliaris or phthiriasis palpebrarum.
The main symptom of infestation with crab lice is itching, usually in the pubic-hair area, resulting from hypersensitivity to
louse saliva, which can become stronger over two or more weeks following initial infestation. In some infestations, a
characteristic grey-blue or slate coloration appears (maculae caeruleae) at the feeding site, which may last for several days.
Crab lice usually infect a new host only by close contact between individuals, usually through sexual intercourse. Adults are
more frequently infested than children. Non-sexual transmissions may occur among family and roommates through the use
of shared towels, clothing, beds or closets. They can only survive a short time away from the warmth and humidity of the
human body.
It has been suggested that an increasing percentage of humans removing their pubic hair has led to reduced crab louse
populations in some parts of the world. Other lice that infest humans are the body louse and the head louse The claws of
these three species are adapted to attachment to specific hair diameters.
Pubic lice are not known to transmit disease. Adult pubic lice are 1.1–1.8 mm in length. The pubic hair can typically host up to
a dozen on average. Pubic lice typically are found attached to hair in the pubic area but sometimes are found on coarse hair
elsewhere on the body (for example, eyebrows, eyelashes, beard, mustache, chest, armpits, etc.). Crab lice attach to pubic
hair that is thicker than other body hair because their claws are adapted to the specific diameter of pubic hair. Pubic lice

infestations (pthiriasis) are usually spread through sexual contact. The crab louse can travel up to 10 inches on the body. Pubic
lice infestation is found worldwide and occurs in all races and ethnic groups and in all economic levels. Pubic lice usually are
spread through sexual contact and are most common in adults. Occasionally pubic lice may be spread by close personal
contact or contact with articles such as clothing, bed linens, and towels that have been used by an infested person. Pubic lice
found on the head or eyelashes of children may be an indication of sexual exposure or abuse. Pubic lice do not transmit
disease; however, secondary bacterial infection can occur from scratching of the skin.They are much broader in comparison
to head and body lice. Adults are found only on the human host and require human blood to survive. If adults are forced off
the host, they will die within 24–48 hours without a blood feeding.
Symptoms of crab louse infestation in the pubic area include itching, redness and inflammation. These symptoms cause
increased blood circulation to the skin of the pubic region creating a blood-rich environment for the crab louse. Pubic lice
infestation can also be diagnosed by identifying the presence of nits or eggs on the pubic hair. When clinicans find the crab
louse on one family member they often request to examine other members of the family for similar symptoms of infestation.
If a clinician suspects the presence of the louse, they may be able to identify the nits or eggs under magnification.

3. VIRAL
I. HERPES SIMPLEX
Herpes simplex is a viral disease caused by the herpes simplex virus. Infections are categorized based on the part of the body
infected. Oral herpes involves the face or mouth. It may result in small blisters in groups often called cold sores or fever
blisters or may just cause a sore throat. Genital herpes, often simply known as herpes, may have minimal symptoms or form
blisters that break open and result in small ulcers. These typically heal over two to four weeks. Tingling or shooting pains may
occur before the blisters appear. Herpes cycles between periods of active disease followed by periods without symptoms.
The first episode is often more severe and may be associated with fever, muscle pains, swollen lymph nodes and headaches.
Over time, episodes of active disease decrease in frequency and severity. Other disorders caused by herpes simplex include:
herpetic whitlow when it involves the fingers, herpes of the eye, herpes infection of the brain, and neonatal herpes when it
affects a newborn, among others.
SIGNS AND SYMPTOMS

CONDITION DESCRIPTION
Herpetic Herpetic gingivostomatitis is often the initial presentation during the first herpes infection. It is
gingivostomatitis of greater severity than herpes labialis, which is often the subsequent presentations.
Herpes labialis Infection occurs when the virus comes into contact with oral mucosa or abraded skin.
Herpes genitalis When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is
clusters of inflamed papules and vesicles on the outer surface of the genitals resembling cold
sores.
Herpetic whitlow and Herpes whitlow is a painful infection that typically affects the fingers or thumbs. On occasion,
herpes gladiatorum infection occurs on the toes or on the nail cuticle. Individuals who participate in contact sports
such as wrestling, rugby, and football(soccer), sometimes acquire a condition caused by HSV-1
known as herpes gladiatorum, scrumpox, wrestler's herpes, or mat herpes, which presents as
skin ulceration on the face, ears, and neck. Symptoms include fever, headache, sore throat, and
swollen glands. It occasionally affects the eyes or eyelids.
Herpesviral encephalitis A herpetic infection of the brain thought to be caused by the transmission of virus from a
and herpesviral peripheral site on the face following HSV-1 reactivation, along the trigeminal nerve axon, to the
meningitis brain. HSV is the most common cause of viral encephalitis. When infecting the brain, the virus
shows a preference for the temporal lobe. HSV-2 is the most common cause of Mollaret's
meningitis, a type of recurrent viral meningitis.

Herpes esophagitis Symptoms may include painful swallowing (odynophagia) and difficulty swallowing (dysphagia).
It is often associated with impaired immune function (e.g. HIV/AIDS, immunosuppression in
solid organ transplants).
Other
Neonatal herpes simplex is a HSV infection in an infant. It is a rare but serious condition, usually caused by vertical transmission
of HSV-1 or -2) from mother to newborn. During immunodeficiency, herpes simplex can cause unusual lesions in the skin.
One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut. Herpetic
sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicles. Eczema herpeticum is an infection
with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous
areas.
Herpetic keratoconjunctivitis, a primary infection, typically presents as swelling of the conjunctiva and eyelids
(blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea.
Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle.
Bell's palsy
Although the exact cause of Bell's palsy—a type of facial paralysis—is unknown, it may be related to reactivation of HSV-1.
This theory has been contested, however, since HSV is detected in large numbers of individuals having never experienced
facial paralysis, and higher levels of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy compared
to those without. Antivirals may improve the condition slightly when used together with corticosteroids in those with severe
disease.
Alzheimer's disease
HSV-1 has been proposed as a possible cause of Alzheimer's disease. In the presence of a certain gene variation (APOE-
epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one's risk of
developing Alzheimer's disease. The virus interacts with the components and receptors of lipoproteins, which may lead to its
development
DIAGNOSIS
Primary orofacial herpes is readily identified by clinical examination of persons with no previous history of lesions and contact
with an individual with known HSV-1 infection. The appearance and distribution of sores in these individuals typically presents
as multiple, round, superficial oral ulcers, accompanied by acute gingivitis. Adults with atypical presentation are more difficult
to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms
from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth,
primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer)
also resemble intraoral herpes, but do not present a vesicular stage.

Genital herpes can be more difficult to diagnose than oral herpes, since most HSV-2-infected persons have no classical
symptoms. Further confusing diagnosis, several other conditions resemble genital herpes, including fungal infection, lichen
planus, atopic dermatitis, and urethritis.[34] Laboratory testing is often used to confirm a diagnosis of genital herpes.
Laboratory tests include culture of the virus, direct fluorescent antibody (DFA) studies to detect virus, skin biopsy, and
polymerase chain reaction to test for presence of viral DNA. Although these procedures produce highly sensitive and specific
diagnoses, their high costs and time constraints discourage their regular use in clinical practice.
It should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, which is
caused by varicella zoster virus. The differential diagnosis includes hand, foot and mouth disease due to similar lesions on
the skin.
MANAGEMENT
No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity
of outbreaks. Analgesics such as ibuprofen and paracetamol (acetaminophen) can reduce pain and fever. Topical anesthetic
treatments such as prilocaine, lidocaine, benzocaine, or tetracaine can also relieve itching and pain.
Antivirals
Several antiviral drugs are effective for treating herpes, including acyclovir, valaciclovir (valacyclovir), famciclovir, and
penciclovir. Acyclovir was the first discovered and is now available in generic. Valacyclovir is also available as a generic and is
slightly more effective than aciclovir for reducing lesion healing time.
Evidence supports the use of acyclovir and valacyclovir in the treatment of herpes labialis as well as herpes infections in
people with cancer. The evidence to support the use of acyclovir in primary herpetic gingivostomatitis is weaker.
Topical
A number of topical antivirals are effective for herpes labialis, including acyclovir, penciclovir, and docosanol .
II. MOLLUSCUM CONTANGIOSUM

Molluscum contagiosum (MC), sometimes called water warts, is a viral infection of the skin that results in small, raised, pink
lesions with a dimple in the center. They may occasionally be itchy or sore. They may occur singly or in groups. Any area of
the skin may be affected, with abdomen, legs, arms, neck, genital area, and face being most common. Onset of the lesions is
around 7 weeks after infection. It usually goes away within a year without scarring.
SIGNS AND SYMPTOMS

Molluscum contagiosum lesions are flesh-colored, dome-shaped, and pearly in appearance. They are often 1–5 mm in
diameter, with a dimpled center. Molluscum lesions are most commonly found on the face, arms, legs, torso, and armpits in

children. Adults typically have molluscum lesions in the genital region and this is considered to be a sexually transmitted
infection; because of this, if genital lesions are found on a child, sexual abuse should be suspected. These lesions are generally
not painful, but they may itch or become irritated. Picking or scratching the bumps may lead to a spread of the viral infection
responsible for molluscum contagiosum, an additional bacterial infection, and scarring. In about 10% of the cases, eczema
develops around the lesions.
Individual molluscum lesions may go away on their own within two months and generally clear completely without treatment
or scarring in six to twelve months. Mean durations for an outbreak are variously reported from 8 to about 18 months, but
durations are reported as widely as 6 months to 5 years, lasting longer in immunosuppressed individuals.
TRANSMISSION
Molluscum contagiosum is extremely contagious. Transmission of the molluscum contagiosum virus can occur many different
ways including direct skin contact (e.g., contact sports or sexual activity), contact with an infected surface (fomite), or
autoinoculation (self-infection) by scratching or picking molluscum lesions and then touching other parts of the skin not
previously affected by the virus. Children are particularly susceptible to autoinoculation and may have widespread clusters of
lesions.
The viral infection is limited to a localized area on the topmost layer of the superficial layer of the skin. Once the virus-
containing head of the lesion has been destroyed, the infection is gone. The central waxy core contains the virus.
DIAGNOSIS
Diagnosis is made on the appearance; the virus cannot routinely be cultured. The diagnosis can be confirmed by excisional
biopsy.
Histologically, molluscum contagiosum is characterized by molluscum bodies in the epidermis, above the stratum basale,
which consist of large cells with abundant granular eosinophilic cytoplasm (accumulated virions) and a small peripheral
nucleus.
MANAGEMENT
Because molluscum contagiosum is usually self-limiting (resolving without treatment) and treatment options can cause
discomfort to children, initial recommendations are often to simply wait for the lesions to resolve on their own. Current
treatment options are invasive, requiring tissue destruction and patient discomfort.
Bumps located in the genital area may be treated in an effort to prevent them from spreading. When treatment has resulted
in elimination of all bumps, the infection has been effectively cured and will not reappear unless the person is reinfected.
Medications
For mild cases, over-the-counter wart medicines, such as salicylic acid may shorten infection duration. Daily topical application
of tretinoin cream may also trigger resolution. These treatments require several months for the infection to clear, and are
often associated with intense inflammation and possibly discomfort.

Studies have found cantharidin to be an effective and safe treatment for removing molluscum contagiosum. This medication
is usually well-tolerated though mild side effects such as pain or blistering are common. There is no high-quality evidence for
cimetidine. However, oral cimetidine has been used as alternative treatment for pediatric population as it is more difficult to
use more invasive and discomforting application.
Imiquimod
Imiquimod is a form of immunotherapy initially proposed as a treatment for molluscum based on promising results in small
case series and clinical trials.
Surgery
Surgical treatments include cryosurgery, in which liquid nitrogen is used to freeze and destroy lesions, as well as scraping
them off with a curette. Application of liquid nitrogen may cause burning or stinging at the treated site, which may persist
for a few minutes after the treatment. With liquid nitrogen, a blister may form at the treatment site, but it will slough off in
two to four weeks. Cryosurgery and curette scraping can be painful procedures and can result in residual scarring.
Laser
A 2014 systematic review of case reports and case series concluded that the limited available data suggest pulsed dye laser
therapy is a safe and effective treatment for molluscum contagiosum and is generally well-tolerated by children.[28] Side
effects seen with pulsed dye laser therapy included mild temporary pain at the site of therapy, bruising (lasting up to 2–3
weeks), and temporary discoloration of the treated skin (as long as 1–6 months). No cases of permanent scarring have been
reported. As of 2009, however, there is no evidence for genital lesions.
PROGNOSIS
Most cases of molluscum contagiosum will clear up naturally within two years (usually within nine months). So long as the
skin growths are present, there is a possibility of transmitting the infection to another person. When the growths are gone,
the possibility of spreading the infection is ended.
Unlike herpesviruses, which can remain inactive in the body for months or years before reappearing, molluscum contagiosum
does not remain in the body when the growths are gone from the skin and will not reappear on their own.

4. FUNGAL
CANDIDIASIS
Candidiasis is a fungal infection due to any type of Candida (a type of yeast). When it affects the mouth, it is commonly called
thrush. Signs and symptoms include white patches on the tongue or other areas of the mouth and throat. Other symptoms
may include soreness and problems swallowing. When it affects the vagina, it is commonly called a yeast infection. Signs and
symptoms include genital itching, burning, and sometimes a white "cottage cheese-like" discharge from the vagina. Less
commonly the penis may be affected, resulting in itchiness. Very rarely, the infection may become invasive, spreading to
other parts of the body. This may result in fevers along with other symptoms depending on the parts involved.
More than 20 types of Candida can cause infection with Candida albicans being the most common. Infections of the mouth
are most common among children less than one month old, the elderly, and those with weak immune systems. Conditions
that result in a weak immune system include HIV/AIDS, the medications used after organ transplantation, diabetes, and the
use of corticosteroids. Other risks include dentures and following antibiotic therapy. Vaginal infections occur more commonly
during pregnancy, in those with weak immune systems, and following antibiotic use. Risk factors for invasive candidiasis
include being in an intensive care unit, following surgery, low birth weight infants, and those with weak immune systems.
Efforts to prevent infections of the mouth include the use of chlorhexidine mouth wash in those with poor immune function
and washing out the mouth following the use of inhaled steroids. Little evidence supports probiotics for either prevention or
treatment even among those with frequent vaginal infections. For infections of the mouth, treatment with topical clotrimazole
or nystatin is usually effective. By mouth or intravenous fluconazole, itraconazole, or amphotericin B may be used if these do
not work. A number of topical antifungal medications may be used for vaginal infections including clotrimazole. In those with
widespread disease, an echinocandin such as caspofungin or micafungin is used. A number of weeks of intravenous
amphotericin B may be used as an alternative. In certain groups at very high risk, antifungal medications may be used
preventatively.
Infections of the mouth occur in about 6% of babies less than a month old. About 20% of those receiving chemotherapy for
cancer and 20% of those with AIDS also develop the disease. About three-quarters of women have at least one yeast infection
at some time during their lives. Widespread disease is rare except in those who have risk factors.

SUMMARY OF STIs

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DCM 3106: DERMATO-VENEREOLOGY I

WEEK 2 History taking and physical examination in dermatology

CORE READING MATERIALS

THE CUTANEOUS MEMBRANE

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THE SUBCUTANEOUS TISSUE

FUNCTIONS OF THE SKIN

FACTORS AFFECTING SKIN PENETRATION

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PAST MEDICAL, SURGICAL HISTORY

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c) Inspect: entire skin

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If inflammation or carcinoma: palpate draining nodes for the lesions.

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BACTERIAL SKIN CONDITIONS

ABSSSI are complex bacterial skin infections. They include

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Signs and symptoms

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Signs and symptoms

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Signs and symptoms

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VIRAL SKIN INFECTIONS

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PARASITIC SKIN INFECTIONS

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Focal hypopigmentation is most commonly a consequence of

Diffuse hypopigmentation or depigmentation is most often caused by

SYMPTOMS AND SIGNS

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DIAGNOSIS: CLINICAL EVALUATION

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Rarely, a cause cannot be identified.

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TOXIC EPIDERMAL NECROLYSIS (TEN)

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Many suspected aetiologic factors have been reported to cause EM

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ERYTHEMA GYRATUM REPENS

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SWEET’S SYNDROME (ACUTE FEBRILE NEUTROPHILIC DERMATOSIS)

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TROUSSEAU SIGN OF MALIGNANCY

There are two main types of pyoderma gangrenosum:

Other variations are: