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Lesson 1

June 27, 2024

Lesson 1

Theme: Anatomy, histology, and physiology of the skin. Skin lesions and methods of examination of patients with skin diseases. Features of clinical motion of scabies, pediculosis and demodecosis. Principles of their differential diagnosis, prophylaxis, and treatment.

1.http://emedicine.medscape.com/article/1294744-overview

2.http://www.youtube.com/watch?v=AvbDyOIZuGY

The human skin is the outer covering of the body. In humans, it is the largest organ of the integumentary system. The skin has multiple layers of ectodermal tissue and guards the underlying muscles, bones, ligaments and internal organs.^[1] Human skin is similar to that of most other mammals, except that it is not protected by a pelt. Though nearly all human skin is covered with hair follicles, it can appear hairless. There are two general types of skin, hairy and glabrous skin. The adjective cutaneous literally means “of the skin” (from Latin cutis, skin).

Because it interfaces with the environment, skin plays a key role in protecting the body against pathogens and excessive water loss. Its other functions are insulation, temperature regulation, sensation, synthesis of vitamin D, and the protection of vitamin B folates. Severely damaged skin will try to heal by forming scar tissue. This is often discolored and depigmented.

In humans, skin pigmentation varies among populations, and skin type can range from dry to oily. Such skin variety provides a rich and diverse habitat for bacteria which number roughly at 1000 species from 19 phyla.

Human skin is a remarkable organ, the body’s largest, but it is often taken for granted. Most people are content to let skin be until dryness, oiliness, a rash or a wrinkle rouses attention. But once they understand how skin functions, many reconsider the importance of the skin and the quality and content of the skin care products they use. Using natural skin care can make more of a difference than most folks realize.

Consider these facts:
1 . An adult’s skin comprises between 15 and 20 percent of the total body weight.
2. Each square centimeter has 6 million cells, 5,000 sensory points, 100 sweat glands and 15 sebaceous glands.

Skin is constantly being regenerated. A cell is born in the lower layer of the skin called the dermis, which is supplied with blood vessels and nerve ending. The cell migrates upward for about two weeks until it reaches the bottom portion of the epidermis, which is the outermost skin layer. The epidermis doesn’t have blood vessels but does have nerve endings. The cell spends another two weeks in the epidermis, gradually flattening out and continuing to move toward the surface. Then it dies and is shed.

Two billion to 3 billion skin cells are shed daily. The body expends this effort to replace skin every month because the skin constitutes the first line of defense against dehydration, infection, injuries and temperature extremes. Skin cells can detoxify harmful substances with many of the same enzymatic processes the liver uses. The unbroken surface also prevents infectious organisms from penetrating into systemic circulation. As gatekeeper, the skin absorbs and uses nutrients applied topically. Because it cannot completely discriminate, the skin may absorb the synthetic chemicals often present in soaps and lotions and other skin care products, which at best it has no use for and at worst can be toxic or irritating.

Most of our site visitors are committed to natural foods and remedies, but many aren’t as selective when it comes to personal skin care products. These otherwise savvy shoppers might purchase any sale shampoo, skin care cleanser or lotion. But because new skin is constantly being generated and because it plays such an important protective role, it makes sense to choose nourishing natural skin care products.

Ten interesting facts you should know about Human Skin:

1. The skin is the bodies largest organ.

2. The skin’s scientific name is Cutaneous Membrane.

3. It is constantly shedding dead cells. The Average person sheds approximately 1 1/2 Ibs of dead skin cells each year.

4. An average adult has more than 20 square feet of skin. A square inch of the human body has approximately 19,000,000 skin cells.and up to 300 sweat glands.

5. The skin’s thinnest area on the human body, is on the eyelids.

6. Contains a pigment called Melanin. The more melanin the darker the skin, less makes it lighter.

7. It is made up of three layers. The Epidermis is the outer layer, the Dermiss is the middle layer and Subcutaneous is the inner most layer.

8. It protects the body against invasion of bacteria and other foreign objects.

9. It helps to regulate body temperature. Goose bumps are little pimples that helps keep a layer of warm air over your body.

10. Contrary to what is believed, dust is not made up mostly of dead skin cells, there are vastly more sources of dust pollutants floating around the air.

Basic Skin Functions

Protection and Immune Response

o The skin is the first line of defense against pathogens and toxins in the environment. When a pathogen, such as a virus or bacteria, is found by Langerhans cells, a specialized dendritic cell, the cell begins the process to destroy the pathogen and remove it from the body.

The protective functions of the skin

1.The skin is the largest human organ. Its major task is to serve as a barrier to the outside world and to protect the body from influences from the environment. It further protects the body from drying out overheating and does not allow undesired germs to penetrate into it. The skin is closely connected with the psyche. It receives touch stimuli through the sense organ and reacts on pressure and temperature.

2. In our schematic representation of the skin, the major skin functions are shown. Primarily, the skin is built up as a protective organ and has a metabolism of its own. The skin is very sensitive to environmental influences, different temperatures, cold, (see diagram (1)) and solar irradiation (2), which leads to sweat formation (sweat area with bacteria metabolism products (3)).

3. Our cross-section of the skin shows four skin compartments and penetration routes. The outer layer is the epidermis with keratinocytes and horny cells which represent the surface. Below, the basal membrane is found between the dermis and epidermis, which is connected with the dermis through collagen structures. Under the basal membrane, the dermis, nerve endings, lymph vessels and capillaries of the blood vessel system are located. The hypodermis is the interior skin layer under the hair papillaries and consists of connective and adipose tissues. Temperature regulation is its main task.

4.Thus, another major function of the skin is temperature regulation. Through widening or narrowing of the blood vessels in the skin and by secretion of liquids over the skin’s glands, the skin has an influence on the body temperature.

5.The skin has a barrier function. The pH-value of intact skin is 5.5. This is due to endogenous acid substances in sweat, sebaceous and horny cells. The significance of this acid property of the skin’s surface becomes obvious by the so-called “acid protection layer”.

6.This acid protection layer or hydro lipidic film plays a major role in the skin’s protectioext to the keratinized cell layer of the epidermis. It is formed by secreted sebum and sweat glands and the lipids of the horny layer and lies directly on the horny layer (stratum corneum), the outer visible part of the epidermis. It has antimicrobial effects and protects the skin from alkaline and acid substances. If the acid protection layer is intact, it keeps the bacterial decomposition of sweat components low.

7.The horny layer protects the skin from penetrating substances and mechanical influences thus preventing the organism from losing water and electrolytes. The openings which are formed by appendages such as hair, sebaceous and sweat glands are further penetration routes.

8.Among the further major tasks of the skin is its function as a sense organ and its function to communicate with the environment. By means of a series of receptors such as warmth and cold receptors or intraepithelial nervous endings, which, in total, turn the skin into a sense organ, stimuli such as cold, warmth and pain are perceived.

9.Further sense organs are Vater-Pacini corpuscules (pressure and tension sensors)), Meissner’s touch corpuscules or touch discs (receptors for touch), corpuscules of Ruffini (receptors for expansion) and Krause end bulbs (mechanoreceptors).

10.Through blushing, paling and other expressions which are regulated by the autonomic nervous fibres, the skin functions as a sense organ and communication system, which is closely connected with the autonomic nervous system.

THE IMMUNE RESPONSE

Primary Immune Response

The first time your body is exposed to particular viruses or bacteria, it takes time for your
immune system to recognize the invading organisms and to figure out how to kill them.
During this elapsed time, bacteria and viruses grow exponentially, thus increasing the
amount of time it takes to completely eliminate the infection.

A cut in the skin damages cells and allows bacteria into the body signaling an immune
response from macrophages and other scavenger immune cells.

Mast cells release chemicals that trigger inflammation, allow-ing other immune cells to
rush to the problem area.

Before reinforcements arrive, macrophages and other prestationed immune cells start
attacking bacteria, chop them up into bits called antigens.

They are then transported to lymph nodes where these macrophages attach to B cells
and T cells. B cells begin producing antibodies specifically for the particular antigens
or germs the body is exposed to.

The antibodies trigger responses from certain immune cells like NK cells, macrophages
and killer T cells to engulf and kill the bacteria-infected cells.

Helper T cells signal the antibodies and killer T cells to go directly to the wound.

While the immune cells are taking care of the germs, other cells called platelets begin
healing the wound by forming clots which close the wound.

Secondary Immune Response

The second time the body is exposed to a particular virus or bacteria, the immune system
recognizes the invading organism more quickly and immediately knows how to fight it off.
Because the amount of time in these steps is shorter, the infection can be eliminated
more quickly. Transfer Factor triggers a secondary immune response by borrowing the
immune memory of the cow or the chicken.

A cut in the skin damages cells and allows bacteria into the body signaling an immune
response from macrophages and other scavenger immune cells.

Mast cells release chemicals that trigger inflammation, allowing other immune cells to
rush to the problem area.

Before reinforcements arrive, macrophages and other pre-stationed immune cells
start attacking bacteria, chop them up into bits called antigens.

B cells, set in motion by previous immune responses, begin producing antibodies
specifically for the particular antigens or germs the body is exposed to. The antibodies
trigger responses from certain immune cells like NK cells, macrophages & killer T cells
to engulf and kill the bacteria-infected cells.

Helper T cells signal the antibodies and killer T cells to go directly to the wound.

While the immune cells are taking care of the germs, other cells called platelets begin
healing the wound by forming clots which close the wound.

Body Temperature Regulation

http://www.youtube.com/watch?v=KJZCOjdG8eA

o Skin controls body temperature by contracting or expanding the blood vessels in the skin. Dilated blood vessels release heat from the body. Contracted blood vessels restrict heat loss. Increased perspiration cools the body while decreased perspiration keeps the body warmer.

Evaporation Control

o Skin provides a barrier to prevent fluid loss and dehydration.

Storage and Nutrient Synthesis

o Skin stores water in addition to lipids which are fat-soluble molecules such as fats, waxes, cholesterol and vitamins A, D, E and K. Interaction with UV light synthesis vitamin B and vitamin D.

Excretion

o The skin excretes urea and excess minerals. In addition, new studies show that skin excretes pheromones and may have an impact on hormonal balance of the opposite gender.

Absorption

Iv been reaserching and would like to share a few things iv found out:looking into the 2 sides of what the skin will absorbe (io paticular order)-Please note this is not My opinion merly what i have found on different websites with links thankyou.+ please feel free to add your findings.

Absorption is a route by which substances can enter the body through the skin. Along with inhalation, ingestion and injection, dermal absorption is a route of exposure for toxic substances and route of administration for medication. Absorption of substances through the skin depends on a number of factors, the most important of which are concentration, duration of contact, solubility, physical condition of the skin and part of the body exposed. Certain substances called carriers can be used to greatly increase the amount of another substances that is able to penetrate the skin. Dimethyl sulfoxide (DMSO) is a carrier that is frequently used to transport medication through the skin. This allows treatment to be localized, unlike with ingestion.
http://en.wikipedia.org/wiki/Absorption_%28skin%29

An absorption base is used to enable beneficial herbs and ingredients, collagen and vitamins to be absorbed into the surface of the skin. An absorption base allows the active ingredients of a product to penetrate into the skin. Essential oils are an absorption base that can be a mixture of alcohols, acids, oxides, lanolin, esters, sulfur compounds, ketones, ethers, ketones or aldehydes. A good absorption base is fatty acids vitamins and it also moisturizes the skin.

http://www.vegetarian-restaurants.net/Ad…smetic.htm

Essential Oils Penetrate.

The penetrating characteristic of essential oils greatly enhances their ability to be effective. Essential oils will penetrate into the body when applied to the skin. Placed on the foot they will be distributed to every cell in the body in 21 minutes. They will even penetrate a finger or toe nail to treat fungus underneath.
Essential oils last 20 minutes in the body.

Oils are a precursor to set up stage for action and a catalyst to do the work (the bloodstream). Oils go where the need is present and are activated in that area. Testing on thyroid, heart and pancreas showed that the oils reached these organs in 3 seconds. When layered, one oil applied over another, it is faster. The body absorbs the oils fasted by breathing and second fastest by applying to the feet or ears. Essential Oils also cross the blood brain barrier. They piggy-back the energy waves to get into the cells.

http://www.therapure.com/yleo/eowhatr.htm

Compared to other body structures, the skin is unique in being perpetually exposed to the environment.
The rate of dermal absorption of a substance is proportional to both the concentration of the substance and the surface area over which it is applied. The wider the contact area and the more concentrated the substance, the greater will be the absorption.
The thickness of the skin, especially the stratum corneum, also determines the degree to which substances are absorbed.

http://www.cape.ca/children/derm2.html

Some of the aromatic ‘essential’ oils used in aromatherapy do have well-documented therapeutic actions. However, many of the oils for which aromatherapists claim physiological medical activity, in fact possess no recorded historical medicinal actions
Most aromatherapists claim explicit physical effects after massaging with oils, for example: “Fennel is diuretic,” “Geranium regulates the hormonal system,” “Grapefruit is good for cellulite.” However, none of these effects have been proven when these oils are applied to the skin during massage.
One example of the misleading hype is found with Fennel oil. It is well known for producing an increase in urine output when it is taken as a medicine. However, when the volume of fennel oil used in the average massage is applied, it is doubtful that enough can be absorbed through the skin to elicit any such diuretic action. If very large amounts are used on the skin, or it is occluded – such as with compresses – or the essential oil is used in hot humid environments, then I am prepared to accept some oil may get into the subcutaneous tissues.

Skin absorption studies at the University of Michigan demonstrated that jojoba is quickly absorbed into the skin, which is apparently via the transappendegeal mechanism and occurs through the pores and hair follicles – but because it is so rapidly absorbed, the pores and hair follicles remain open and thus maintain their proper functioning ability.

http://www.ageless.co.za/herb-jojoba.htm#Properties

your skin absorbs up to 60% of whatever is applied – including toxin

http://www.newforestsoaps.co.uk/yourskin.htm

Human skin will not absorb most common waters because of incorrect application and an incompatible pH balance.
http://www.naturesmist.com/skinfunc.html

The skin can absorb chemicals, not just nicotine from patches, but harmful toxins and carcinogens, and yet these can be found in many personal care products.
http://www.bodyandhaircare.co.uk/skincarepage.htm

Nutrition for healthy skin

Vitamin A, also known as retinoids, benefits the skin by normalizing keratinization, downregulating sebum production which contributes to acne, and reversing and treating photodamage, striae, and cellulite.

Vitamin D and analogs are used to downregulate the cutaneous immune system and epithelial proliferation while promoting differentiation.

Vitamin C is an antioxidant that regulates collagen synthesis, forms barrier lipids, regenerates vitamin E, and provides photoprotection.

Vitamin E is a membrane antioxidant that protects against oxidative damage and also provides protection against harmful UV rays.

Skin overview

Four Steps for a Healthy Skin

1. Cleansing. Find a good Cleanser that your skin responds well to, and stick with it. Choose a Creamy Cleanser if you have dry skin or a Clear Cleanser if you have oily skin. Be careful not to cleanse too often, you risk over-cleansing skin, you really only need to wash your face at night to remove makeup and sunscreen, which can clog pores. If you have dry skin, consider cold cream. Use warm water to loosen dirt and clogged pores. Use a dime-sized bit of cleanser, and then rinse with cool or lukewarm water. In the morning, a splash of lukewarm water is all you need. Never wash your face with hot or cold water (both can cause broken capillaries).

2. Exfoliate. If you start properly exfoliating your skin, you will notice an almost immediate difference. Put a dab of cleanser on a damp washcloth and massage the cleanser into my skin in a circular motion. After a quick rinse, any sign of dead skin is erased. You can also exfoliate skin via microdermabrasion, chemical peels and Retinoids. Scrubs work by removing the top layer of dead skin cells that tend to dull your complexion. Make sure you use a gentle scrub with tiny grains. Big grains in cheap scrubs can tear skin and cause more harm than good. Retinoids (such as Retin-A or the more moisturizing Renova) also work by removing the top layer of dead skin cells while also generating collagen in the skin. Skincare experts consider Retinoids to be a miracle skin saver.

3. Moisturizing. if you have dry skin, you should invest in a Basic Moisturizer. How much should you moisturize? Your skin will tell you. When your skin is tight, it’s crying out for moisture. Be careful not to over-moisturize — this can clog pores.

4. Sun Screen. Major cause of wrinkles is sun damage, so it’s important to use a sunscreen of at least 30 SPF from your early years on even in winter and on cloudy days. A great trick is to purchase two moisturizers: One for night and one for day that includes UV protection. Don’t use moisturizers with sunscreen at night, make sure it contains Mexoryl or Helioplex.

Hygiene and skin care

The skin supports its own ecosystems of microorganisms, including yeasts and bacteria, which cannot be removed by any amount of cleaning. Estimates place the number of individual bacteria on the surface of one square inch (6.5 square cm) of human skin at 50 million, though this figure varies greatly over the average 20 square feet (1.9 m²) of human skin. Oily surfaces, such as the face, may contain over 500 million bacteria per square inch (6.5 cm²). Despite these vast quantities, all of the bacteria found on the skin’s surface would fit into a volume the size of a pea. In general, the microorganisms keep one another in check and are part of a healthy skin. When the balance is disturbed, there may be an overgrowth and infection, such as when antibiotics kill microbes, resulting in an overgrowth of yeast. The skin is continuous with the inner epithelial lining of the body at the orifices, each of which supports its own complement of microbes.

Proper skin hygiene is important because unclean skin favors the development of pathogenic organisms. The dead cells that continually slough off the epidermis mix with the secretions of the sweat and sebaceous glands and the dust found on the skin form a filthy layer on its surface. If not washed away, the slurry of sweat and sebaceous secretions mixed with dirt and dead skin is decomposed by bacterial flora, producing a foul smell. Functions of the skin are disturbed when it is excessively dirty; it becomes more easily damaged, the release of antibacterial compounds decreases, and dirty skin is more prone to develop infections.

Cosmetics should be used carefully on the skin because these may cause allergic reactions. Each season requires suitable clothing in order to facilitate the evaporation of the sweat. Sunlight, water and air play an important role in keeping the skin healthy.

Oily skin

Oily skin is caused by over-active sebaceous glands, that produce a substance called sebum, a naturally healthy skin lubricant.^[1] When the skin produces excessive sebum, it becomes heavy and thick in texture. Oily skin is typified by shininess, blemishes and pimples.The oily-skin type is not necessarily bad, since such skin is less prone to wrinkling, or other signs of aging, because the oil helps to keep needed moisture locked into the epidermis (outermost layer of skin).

The negative aspect of the oily-skin type is that oily complexions are especially susceptible to clogged pores, blackheads, and buildup of dead skin cells on the surface of the skin.^[1] Oily skin can be sallow and rough in texture and tends to have large, clearly visible pores everywhere, except around the eyes and neck.

Aging

As skin ages, it becomes thinner and more easily damaged. Intensifying this effect is the decreasing ability of skin to heal itself as a person ages.

Among other things, skin aging is noted by a decrease in volume and elasticity. There are many internal and external causes to skin aging. For example, aging skin receives less blood flow and lower glandular activity.

A validated comprehensive grading scale has categorized the clinical findings of skin aging as laxity (sagging), rhytids (wrinkles), and the various facets of photoaging, including erythema/telangiectasia (redness), dyspigmentation (brown discoloration), solar elastosis (yellowing), keratoses (abnormal growths) and poor texture.

Cortisol causes degradation of collagen, accelerating skin aging.

Anti-aging supplements are used to treat skin aging.

Photoaging

Photoaging has two main concerns: an increased risk for skin cancer and the appearance of damaged skin. In younger skin, sun damage will heal faster since the cells in the epidermis have a faster turnover rate, while in the older population the skin becomes thinner and the epidermis turnover rate for cell repair is lower which may result in the dermis layer being damaged.

Disease

Dermatology is the branch of medicine that deals with conditions of the skin.

Variability in skin tone

Human skin shows high skin colour variety from the darkest brown to the lightest pinkish-white hues. Human skin shows higher variation in colour than any other single mammalian species and is the result of natural selection. Skin pigmentation in humans evolved to primarily regulate the amount of ultraviolet radiation (UVR) penetrating the skin, controlling its biochemical effects.^[16]

The actual skin colour of different humans is affected by many substances, although the single most important substance determining human skin colour is the pigment melanin. Melanin is produced within the skin in cells called melanocytes and it is the main determinant of the skin colour of darker-skinned humans. The skin colour of people with light skin is determined mainly by the bluish-white connective tissue under the dermis and by the haemoglobin circulating in the veins of the dermis. The red colour underlying the skin becomes more visible, especially in the face, when, as consequence of physical exercise or the stimulation of the nervous system (anger, fear), arterioles dilate.

There is a correlation between the geographic distribution of UV radiation (UVR) and the distribution of indigenous skin pigmentation around the world. Areas that highlight higher amounts of UVR reflect darker-skinned populations, generally located nearer towards the equator. Areas that are far from the tropics and closer to the poles have lower concentration of UVR, which is reflected in lighter-skinned populations.

In the same population it has been observed that adult human females are considerably lighter in skin pigmentation that the males. Females need more calcium during pregnancy and lactation. Vitamin D which is synthesized from sunlight helps absorbing calcium. Females evolved to have lighter skin in order to help their bodies absorb more calcium.

Skin Phototype

The amount of melanin pigment in the skin determines an individual’s skin color (skin phototype). Skin pigment can be inherited genetically or can be acquired through various diseases. Hormonal changes during pregnancy can also vary the amount of pigmentation.

The Fitzpatrick Scale is used to classify skin complexion and response to UV exposure. (See table 1, below.) This classification is based on a personal history of sunburning and suntanning.This classification is used clinically for evaluation of facial skin pigmentation before resurfacing procedures and is important for predicting outcomes and adverse effects.

Table 1: The Fitzpatrick Scale

Skin Type	Color	Features
I	White or freckled skin	Always burns, never tans
II	White skin	Burns easily, tans poorly
III	Olive skin	Mild burn, gradually tans
IV	Light brown skin	Burns minimally, tans easily
V	Dark brown skin	Rarely burns, tans easily
VI	Black skin	Never burns, always tans

Alterations in Skin Color

1. Redness or erythema

2. Pallor or blanching

3. Jaundice or yellowish discoloration

4. Bruises or blue-black marks

5. Cyanosis

Pigments

Three pigments contribute to skin color:

1. Melanin – yellow, reddish brown, or black

2. Carotene – orange-yellow

3. Hemoglobin – depending on the amount of oxygen bound

Skin flora

The human skin is a rich environment for microbes. Around 1000 species of bacteria from 19 bacterial phyla have been found. Most come from only four phyla: Actinobacteria (51.8%), Firmicutes (24.4%), Proteobacteria (16.5%), and Bacteroidetes (6.3%). Propionibacteria and Staphylococci species were the main species in sebaceous areas. There are three main ecological areas: moist, dry and sebaceous. In moist places on the body Corynebacteria together with Staphylococci dominate. In dry areas, there is a mixture of species but dominated by b-Proteobacteria and Flavobacteriales. Ecologically, sebaceous areas had greater species richness than moist and dry ones. The areas with least similarity between people in species were the spaces between fingers, the spaces between toes, axillae, and umbilical cord stump. Most similarly were beside the nostril, nares (inside the nostril), and on the back.

Reflecting upon the diversity of the human skin researchers on the human skin microbiome have observed: “hairy, moist underarms lie a short distance from smooth dry forearms, but these two niches are likely as ecologically dissimilar as rainforests are to deserts.”

Structure of the Skin

• Epidermis

– Made up of stratified squamous epithelium that is capable of keratinization (becoming hard and tough)

• Dermis

– Made up of dense connective tissue

– Deep to the dermis is the subcutaneous tissue or hypodermis, essentially adipose tissue (not considered part of the skin).

1. Epidermis

Composed of five zones or layers called strata

Stratum basale

Structure:

LM: –a layer of cuboidal or low columnar cell with a large, pale N

-basophilic cytoplasm

EM: -free ribosome

-keratin filament- tonofilament

-desmosome

function: mitotic activity and proliferation

Stratum spinosum

Structure:

LM: -4-10 layers polygonal cell with large round nucleus

-spinous processes

-slight basophilic cytoplasm

EM: -tonofibrils

-lamellated granules:

/100-300nm membrane-coated

/contain phospholipid and steroid

-intercellular bridges- Desmosome

Stratum granulosum

Structure:

LM: -3-5 layers flattened cell

-muclei begin to degenerate-stained slightly

-keratohyalin granules: basophilic

EM: –keratohyalin granules: with tonofilament insert into them

-lamellated granules: fused with cell membrane

* keratohyalin + tonofilament = keratin

Stratum lucidum

Structure:

LM:

-3-4 layers of cell appear homogeneous and transparent

-no nucleus and organella

-eosinophilic-keratohyalin

-tonofilament embedded in homogeneous matrix

Stratum corneum

Structure:

LM: -several layers horny cell

-died cell- no nucleus and organella

-eosinophilic

-keratin

* desquamation: surface keratin will shed from outer surface

a) Non-keratinised cell:

melanocyte:

structure:

LM: -large cell with long branches

-located among stratum basale cells

EM: –risosome

-RER

-Golgi complexes tyrosine

-melanosome(tyrosinase) →↓

↓ melanin

melanin granules

b) Langerhans cell

Structure:

LM: -deep nucleus, light cytoplasms

-among the spinous cell

-dendritic-typed processes

EM: -lysosome

granule:membrane-coated

/15-30 nm long, 4 nm in D

function:

• antigen presenting cell in skin

• involve in immune reaction

c) Merkel’s cell

Structure:

located in basal layer;

with short processes;

contain many dense-core granules;

chemical synapse: between Merkel’s cell and afferent N;

function: not very clear, may be sensory epithelial cell;

neuroendocrine cell ( APUD, amine precursor uptake and decarboxylation cell).

2. Dermis

Two major regions

PAPILLARY DERMIS

• Upper dermal region

• Uneven and has fingerlike projections called dermal papillae

• Receptors include free nerve ending and Meissner corpuscles (touch receptor)

RETICULAR DERMIS

• Deepest skin layer

• Contains blood vessels, sweat and oil glands, and deep pressure receptors called Pacinian corpuscles

Upper Papillary Layer

Loose connective tissue

Contain protrusions into epidermis called “PAPILLAE”

Fine capillaries to carry waste away + provide nourishment and oxygen

Nerve endings for heat, pain, cold, pressure and touch (Meissner’s corpuscles)

Double row of papillae Þ better gripping by hands and feet + distinctive fingerprint patterns

Reticular Layer

Elastic network of tough collagen fibres interwoven with elastic fibres

Collagenous fibres arranged in special pattern

Incisions made parallel to these lines during surgery Þ wound heals faster

Contains sebaceous and sweat glands, arrector pili muscle and hair follicle

Pacinian corpuscles are distributed through the dermis and function as pressure receptors

Stretch marks and pregnancy due to breaks in collagen and elastic fibres

Dermoepidermal Junction

The dermoepidermal junction is an undulating basement membrane that adheres the epidermis to the dermis. It is composed of 2 layers, the lamina lucida and lamina densa. The lamina lucida is thinner and lies directly beneath the basal layer of epidermal keratinocytes. The thicker lamina densa is in direct contact with the underlying dermis. These structures are the target of immunologic injury in bullous pemphigoid and epidermolysis bullosa.

Dermal papillae from the papillary dermis contain a plexus of capillaries and lymphatics oriented perpendicular to the skin surface. These fingerlike projections are surrounded by similar projections of the epidermis. This highly irregular junction greatly increases the surface area over which oxygen, nutrients, and waste products are exchanged between the dermis and the avascular epidermis.

3. Hypodermis

“Subcutaneous” layer

Thicker than dermis

Thicker in females

Ducts of sweat glands and bases of hair follicles

APPENDAGES OF THE SKIN

CUTANEOUS GLANDS

Exocrine glands that release their secretion to the skin surface via ducts

SEBACEOUS GLANDS

What are Sebaceous Glands?

Sebaceous Glands are very small glands in the skin that are only visible under the microscope. The glands are responsible for depositing an oily secretion on the hairs called sebum.

Where are Sebaceous Glands Located?

Sebaceous Glands can be found in all parts of the skin in the human body except soles and palms. These glands are generally located in the hairy parts of the body. These are connected to the hair follicles over the skin.

The gland can also be found ion-hairy regions of the skin, such as the eyes, nipples, Labia Minora, penis and nose.

Approximately 3 thousand Sebaceous Glands can be found per square inch of the skin. These glands are primarily found on areas like the face, scalp, chest and back. These mature and start active production of sebum when there is an onset of puberty in the person.

Sebaceous Gland Function

Protecting the skin is the main function of Sebaceous Glands. Sebaceous Glands secrete an oily substance known as Sebum that lubricates the hair and skin of mammals. Large quantities of sebum protect skin and hair from water. It reduces the growth of microorganisms anywhere on the skin.

It is only because of the sebum that people can experience a wet skin even when they have not taken bath for days.

What is Sebum?

“Sebum” is the Latin word for “fat”. It is the oily secretion of the Sebaceous Glands which keeps the hair and skin moisturized and prevents them from cracking, turning dry and getting brittle.

The sebum comprises of lipids, wax and clusters of dead fat-producing cells. The percentage breakup of the composition of sebum shows it to be comprised of

Triglycerides – 40%
Wax monoesters – 25%
Free fatty acids – 16%
Squalene – 12%

Sebum is created in the Sebaceous glands. Following production, this oily substance is secreted through a small duct. From the gland it moves up the hair shaft and ultimately arises to the skin surface through the hair follicle. While coming up, it helps to push out any dust particle, germs or skin debris that may have somehow entered into the hair follicle.

It is because of Sebaceous Glands hair follicles remain free from foreign objects. The sebaceous glands can also come over the skin surface because of the follicles. Hair follicles and Sebaceous Sweat Glands are thus dependent on each other.

Sebum is generally odorless. But they can emit some odor while breaking down on the skin.

Sweat glands:

Sweat glands are coiled tubular glands that lie in the dermis (as far as their histological appearance). They fit into the category of merocrine glands based on what they secrete. Take a look at Figure 5.11 on page 143 to see this, because it is important that you understand this terminology since it gets confusing…

Merocrine glands secrete fluids with dissolved material in them. Sweat glands release water with salt and some metabolic wastes in them, so they fit this category. Urea and uric acid can be some of those wastes, and these molecules are “nitrogenous wastes.” These wastes appear when we have to metabolize proteins for use in the production of energy.

The confusing part of this is that there are two types of sweat glands, depending on whether or not they also contain an odor in the sweat and on whether they secrete through a separate pore. Here are the two:

	eccrine sweat glands secrete odorless sweat through a separate pore.
	apocrine sweat glands secrete odorous sweat into a hair follicle.

Regardless of whether we are discussing an eccrine or an apocrine sweat gland, they are both merocrine glands on the basis of what they secrete. The confusing part about this is that “apocrine glands” is the name for the type of glands that secrete cell parts, wherease “merocrine glands” is the name for the type of gland that secretes dissoved materials. Therefore, one might think (incorrectly) that apocrine sweat glands are apocrine glands. They are not. Apocrine sweat glands are merocrine glands. It is one of those bad terminology problems.

Function of sweat glands:

The sweat glands normally release a little fluid all the time, and as this fluid evaporates, your body cools off. These glands can get stimulated to be more active, so that they secrete even more fluid and help us cool off more. The stimulus to the sweat glands occurs when our bodies recognize (through skin temperature nerve endings and/or blood temperature as it courses through our brains) that they are hot.

Hairs and Hair Follicles

• Primarily dead keratinized cells

• Produced by a hair follicle

• Part enclosed in the follicle is called the root

• Part projecting from the surface is called the shaft

• Hair is formed by division of the cells in the growth zone, or hair bulb matrix

• Arrector pili: small bands of smooth muscle cells attached to the hair follicle producing the “goose bumps”

ww.google.com.ua/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CDMQFjAA&url=http%3A%2F%2Fwww.mpsaz.org%2Fwestwood%2Fstaff%2Ftlblondis%2Fclass2%2Fintegumentary%2Ffiles%2Fskin_appendages.ppt&ei=g93xUPqzJMiXtQaV8IAY&usg=AFQjCNFwDD1taTeG7GsQOZCKaouCaF3CtA&sig2=KR2FNBkXtKRK4HSyDu0QBg&bvm=bv.1357700187,d.Yms

NAILS

BURN ASSESSMENT AND MANAGEMENT

References

1. Prost-Squarcioni C. [Histology of skin and hair follicle]. Med Sci (Paris). Feb 2006;22(2):131-7. [Medline].

2. Rabe JH, Mamelak AJ, McElgunn PJ, Morison WL, Sauder DN. Photoaging: mechanisms and repair. J Am Acad Dermatol. Jul 2006;55(1):1-19. [Medline].

3. Baumann L. Skin ageing and its treatment. J Pathol. Jan 2007;211(2):241-51. [Medline].

4. Goldman MP. Shiffman MA, Mirrafati SJ, Lam SM, et al, eds. Simplified Facial Rejuvenation. New York, NY: Springer; 2008:47-50.

APPROACH TO THE PATIENT

HISTORY

n time course of rash

n distribution of lesions

n symptoms (e.g. itch or pain)

n family history (especially of atopy and psoriasis)

n drug/allergy history

n past medical history

n provocating factors (e.g. sunlight or diet)

n previous skin treatments.

EXAMINATION

n Looking at and feeling a rash

n Assessment of nails, hair, and mucosal surfaces, even if these are recorded as unaffected.

n The following terms are used to describe distribution: flexural, extensor, acral (hands and feet), symmetrical, localized, widespread, facial, unilateral, linear, centripetal (trunk more than limbs), annular and reticulate (lacy network or mesh like).

INVESTIGATIONS

Consider the lesion:

Duration:

Onset – sudden versus gradual? Is this an acute presentation or an ongoing chronic problem?
Previous episodes, eg photodermatoses tend to reoccur every spring with the onset of good weather.
Change – fluctuation versus persistence? Consider variation in severity, eg occupational contact allergic dermatitis may improve when on holiday. Urticaria may be quite dynamic in its presentation but others are much more static.

Location: as well as skin, remember mucous membranes. The site of lesions is important. Eczema tends to be on flexural surfaces (in adults and older children) whilst psoriasis tends to be on extensor parts. Lesions may have a specific distribution – around the genitals, in sweaty regions or sun-exposed areas. Has the lesion spread?
Provoking or relieving factors, eg heat and cold may be either aggravating or relieving factors, especially with urticaria, repeated drug exposures with fixed drug eruptions.
Associated symptoms:

Itch – some lesions are renowned for being itchy and others for not being so but this can be misleading. Psoriasis is said to be non-itchy but there may be pruritus in the genital area.
Tenderness – inflammation is often tender.
Bleeding or discharge – bleeding may indicate malignancy and discharge may occur with an infected lesion.
Systemic symptoms such as pyrexia, malaise, joint pain and swelling or weight loss. Some skin lesions are markers for underlying malignancy.^[3]

Response to treatment – both patient and doctor initiated. A number of treatments may have been tried prior to consultation eg antiseptic lotions, calamine, antihistamines, over-the-counter (OTC) steroid or antifungal creams, herbal remedies or medication prescribed for another family member or friend. Complementary medicines such as chinese herbsmay have unknown ingredients and potency. Partially treated lesions are the most difficult to diagnose.

Now focus on the lesion(s):

Note the position of lesions:

Is the distribution symmetrical or asymmetrical? (Symmetrical distribution suggests an endogenous condition such as psoriasis, whilst asymmetry is more typical of an exogenous condition such as tinea.) Some rashes have a characteristic distribution such as with shingles.
Flexor or extensor surfaces?
Areas of friction or pressure?
Sweaty regions?
Exposed regions?
Related to sexual contact? (consider genital lesions but also the lower abdomen and upper thighs).

Note the size of the lesion. Measure for accuracy.
Is it single or multiple?
If a rash exists, what is its morphology? Are individual lesions:

Macular?
Papular?
Vesicular?
Crusty?
Urticarial?

Note colour, shape, regularity or irregularity. Are there areas of inflammation around it? Is the edge clearly demarcated or poorly defined?

http://www.google.com.ua/url?sa=t&rct=j&q=&esrc=s&source=web&cd=4&ved=0CEkQFjAD&url=http%3A%2F%2Fwww.aimshospital.org%2Fhospital%2Finternal_medicine%2Fpresentation%2FDr.Chaitanya%2Flectures%2FPRIMARY_SECONDARY_SKIN_LESIONS_2003.ppt&ei=2uDxUKa8KszKsgbg0oAg&usg=AFQjCNH4NjijYEzFbzGHgFXgK3BENcQlwA&sig2=QeXnIsFaUZaW4mIbIS_WRA&bvm=bv.1357700187,d.Yms

http://www.youtube.com/watch?v=Ap5fJ-A1bIY

PRIMARY MORPHOLOGY

Macules are flat, nonpalpable lesions usually < 10 mm in diameter. Macules represent a change in color and are not raised or depressed compared to the skin surface. A patch is a large macule. Examples include freckles, flat moles, tattoos, port-wine stains, and the rashes of rickettsial infections, rubella, measles, and some allergic drug eruptions.

Papules are elevated lesions usually < 10 mm in diameter that can be felt or palpated. Examples include nevi, warts, lichen planus, insect bites, seborrheic and actinic keratoses, some lesions of acne, and skin cancers. The term “maculopapular” is often loosely and improperly used to describe many red skin rashes; because this term is nonspecific and easily misused, it should be avoided.

Plaques are palpable lesions > 10 mm in diameter that are elevated or depressed compared to the skin surface. Plaques may be flat topped or rounded. Lesions of psoriasis and granuloma annulare commonly form plaques.

Nodules are firm papules or lesions that extend into the dermis or subcutaneous tissue. Examples include cysts, lipomas, and fibromas.

Vesicles are small, clear, fluid-filled blisters < 10 mm in diameter. Vesicles are characteristic of herpes infections, acute allergic contact dermatitis, and some autoimmune blistering disorders (eg, dermatitis herpetiformis).

Bullae are clear fluid-filled blisters > 10 mm in diameter. These may be caused by burns, bites, irritant or allergic contact dermatitis, and drug reactions. Classic autoimmune bullous diseases include pemphigus vulgaris and bullous pemphigoid. Bullae also may occur in inherited disorders of skin fragility.

Pustules are vesicles that contain pus. Pustules are common in bacterial infections, folliculitis, and may arise in some inflammatory diseases including pustular

Wheal (hive) – a firm edematous plaque resulting from infiltration of the dermis with fluid; wheals are transient and may last only a few hours

SECONDARY MORPHOLOGY

Erosion – focal loss of epidermis; erosions do not penetrate below the dermoepidermal junction and therefore heal without scarring.

Fissure – a linear loss of epidermis and dermis with sharply defined, nearly vertical walls.

Atrophy – a depression in the skin resulting from thinning of the epidermis or dermis.

Scar – an abnormal formation of connective tissue implying dermal damage; after injury or surgery scars are initially thick and pink but with time

become white and atrophic.

Excoriation– an injury to a surface of the body caused by trauma, such as scratching, abrasion, or a chemical or thermal burn.

Crust – a collection of dried serum and cellular debris; a scab.

Scales – ecess dead epidermal cells that are produced by abnormal keratinization and shedding The may be fine, as in pityriasis; white and silvery, as in psoriasis; or large and fish-like, as in ichthyosis.

Lichenification – an area of thickened epidermis induced by scratching; the skin lines are accentuated so that the surface looks like a washboard

Burrow – a arrow, elevated, tortuous channel produced by a parasite.

Petechia – Lat. petecchia (plural = petechiae) = spot on skin) is a small (< 3 mm) red or purple bruise. It does not blanch on applying the pressure.

Now touch:

Tenderness.
Warmth.
Site within the skin.
Thickness.
Consistency (hard, soft, firm, fluctuant).
Does firm pressure lead to blanching?
Is it friable? Does it bleed easily?
Scaling – disorders of the epidermis may produce scale, which may be visible, or gentle scratching of the skin may make it apparent.
If appropriate, look to see if there is any evidence of infestation, e.g scabies‘ burrows.
Note hair in the local skin and on the head.
Look at the nails.^[11]
Are mucous membranes involved?^[¹²^] Examine the genitals where appropriate.
Are there regional lymph nodes? This may be relevant for infectious or malignant lesions.

Differential diagnosis

Having completed the full history and examination, it is usually possible to make a firm diagnosis but, if not, it is certainly possible to distil a great deal of information about the condition. Very often the impressive names that dermatologists give to unusual conditions are nothing more than a description in Latin. Beware of the ‘great mimickers’, eg amelanotic melanoma, lupus erythematosus, sarcoid, mycobacteria and cutaneous T-cell lymphoma. Diagnostic tables and algorithms have been developed to complement clinical acumen.

Where a firm diagnosis cannot be made with a reasonable degree of confidence, investigations may be helpful and even a therapeutic trial may be beneficial. However, steroid cream can mask some aspects of a disease and dermatologists often complain of the difficulties of diagnosing partially treated disease. Teledermatology is fundamentally changing primary care’s access to an expert opinion on a skin condition although concerns persist about reduced diagnostic reliability and the ongoing need for face-to-face consultations, particularly in the diagnosis of skin malignancies.^[¹³^]

One of the most important decisions to make about a skin lesion is whether or not it is malignant.^[¹⁴^] There must be a high index of suspicion and absolute certainty is rare. For pigmented lesions, change is an important element in diagnosing malignant melanoma. Current guidelines suggest assessing on a weighted 7-point scale:^[¹⁵^]

Major features of the lesions: (score 2 points each)

Change in size
Irregular shape
Irregular colour

Minor features of the lesions: (score 1 point each)

Largest diameter 7 mm or more
Inflammation
Oozing
Change in sensation

Suspicion is greater for lesions scoring 3 points or more but, if there are strong concerns, any one feature is sufficient to prompt urgent referral, as should:

Any new solitary nodule or plaque regardless of colour where a benign diagnosis (eg a dermatofibroma) cannot be made with confidence. Half of nodular melanomas are hypomelanotic or amelanotic and may present as a pink nodule.
A new pigmented line in a nail.
Lesions growing under a nail.
Pigmented lesions on mucosal surfaces.

INVESTIGATIONS

Swabs

These can be taken for bacteriology and virology.

Skin scrapings

Skin scrapings for microscopy can be useful to diagnose fungal infections, pityriasis versicolor and ectoparasitic infections such as scabies. For dermatophyte infections, scrape the advancing edge of the scaly lesion carefully.
Nail clippings – ensure a good-sized clipping and scrape from the under the surface of the nail.
Hair root samples can be useful in suspected tinea capitis.

Most laboratories will supply appropriate specimen containers – usually small envelopes with a black interior as it is much easier to see the sample against such a background.

Wood’s light

This is an ultraviolet light (wavelength 360-365 nm) used in a darkened room. It should be held at least 10-15 cm from the skin and time should be allowed for dark accommodation to occur. When shone on some fungal infections, the light causes fluorescence.

Tinea versicolor fluoresces with subtle gold colours.
Erythrasma due to Corynebacterium minutissimum fluoresces a bright coral red.
Tinea capitis caused by Microsporum canis and Microsporum audouinii fluoresce a light bright green but most tinea capitis infections are caused by Trichophyton species that do not fluoresce.

Pseudomonas aeruginosa infection, especially in burns, may provide green-yellow fluorescence.
Vitiligo also fluoresces. Its associated depigmentation can be differentiated from hypopigmented lesions by the ivory-white colour under Wood’s light.
Wood’s light can also be used in the evaluation of pigmented lesions, marking out areas of lentigo maligna or melasma.

Skin biopsy

Biopsy may be used to provide a histopathological specimen to aid diagnosis and guide further management. Always provide relevant history, description and differential diagnosis to assist the histopathologist. Histology may not be able to differentiate between some cases of dysplastic naevi and melanoma so that any case of incompletely excised ‘dysplastic naevus’ should be referred for a further excision.
Shave and punch biopsy techniques can be used. Shave excisions are less demanding technically, and are useful when the lesion is small and the risk of malignancy is low. Punch biopsies remove a core of skin from the epidermis to subcutaneous fat. Ideally the biopsy should include normal skin, part of the lesion and the transition zone. Excisional biopsies aim to remove the entire lesion, with a margin dependent on the risk of malignancy. Its advantage is that the procedure can provide treatment as well as diagnosis for many lesions but it is more demanding of time, equipment and expertise.
Biopsy can also be used for immunofluorescence and culture (eg mycobacterium, leishmaniasis).

Patch and skin prick tests

These are used for the investigation of contact allergic dermatitis and suspected latex and other allergies.

References

1. Courtenay M, Carey N; Nurse-led care in dermatology: a review of the literature. Br J Dermatol. 2006 Jan;154(1):1-6. [abstract]

2. Ersser SJ, Lattimer V, Surridge H, et al; An analysis of the skin care patient mix attending a primary care-based nurse-led NHS Walk-in Centre. Br J Dermatol. 2005 Nov;153(5):992-6. [abstract]

3. Kleyn CE, Lai-Cheong JE, Bell HK; Cutaneous manifestations of internal malignancy: diagnosis and management. Am J Clin Dermatol. 2006;7(2):71-84. [abstract]

4. Ramsay HM, Goddard W, Gill S, et al; Herbal creams used for atopic eczema in Birmingham, UK illegally contain potent corticosteroids. Arch Dis Child. 2003 Dec;88(12):1056-7. [abstract]

5. Slodownik D, Nixon R; Occupational factors in skin diseases. Curr Probl Dermatol. 2007;35:173-89. [abstract]

6. Lupi O, Madkan V, Tyring SK; Tropical dermatology: bacterial tropical diseases. J Am Acad Dermatol. 2006 Apr;54(4):559-78; quiz 578-80. [abstract]

7. Lupi O, Tyring SK, McGinnis MR; Tropical dermatology: fungal tropical diseases. J Am Acad Dermatol. 2005 Dec;53(6):931-51, quiz 952-4. [abstract]

8. Valeyrie-Allanore L, Sassolas B, Roujeau JC; Drug-induced skin, nail and hair disorders. Drug Saf. 2007;30(11):1011-30. [abstract]

9. Dika E, Bardazzi F, Balestri R, et al; Environmental factors and psoriasis. Curr Probl Dermatol. 2007;35:118-35. [abstract]

10. Picardi A, Pasquini P, Abeni D, et al; Psychosomatic assessment of skin diseases in clinical practice. Psychother Psychosom. 2005;74(5):315-22. [abstract]

11. Hinds G, Thomas VD; Malignancy and cancer treatment-related hair and nail changes. Dermatol Clin. 2008 Jan;26(1):59-68, viii. [abstract]

12. Scully C; A review of common mucocutaneous disorders affecting the mouth and lips. Ann Acad Med Singapore. 1999 Sep;28(5):704-7. [abstract]

13. Bowns IR, Collins K, Walters SJ, et al; Telemedicine in dermatology: a randomised controlled trial. Health Technol Assess. 2006 Nov;10(43):iii-iv, ix-xi, 1-39. [abstract]

SCABIES

1.http://www.medscape.com/viewarticle/760499_2

2. http://www.youtube.com/watch?v=UIWsMKeUBQM

Scabies is an intensely pruritic, highly contagious infestation of the skin

Arachnid mite Sarcoptes scabiei, variety hominis.

Originally, scabies was a term used by the Romans to denote any pruritic skin disease.

In the 17th century, Giovanni Cosimo Bonomo identified the mite as one cause of scabies.

The name Sarcoptes scabiei is derived from the Greek words

Sarx (the flesh)

Koptein (to smite or cut) and the

Latin scabere (to scratch). Today, the term scabies refers to the skin lesions produced by this mite.

It has played an important role in world history, with epidemics partially coinciding with military activities and major social upheavals.

Scabies has been recognized as a disease for approximately 2500 years.

It was historically treated with topical sulfur, a treatment still in use today.

Like syphilis, scabies has come to be known as the great imitator.

Its spectrum of clinical manifestations may lead the practitioner to the wrong diagnosis.

The phrase “7 year itch” was first used with reference to persistent, undiagnosed infestation with scabies, not as a movie title.

The mite, S scabiei spreads disease through direct and prolonged contact between hosts.

The mite remains viable for 2-5 days on inanimate objects; therefore, transmission through for mites, such as infected bedding or clothing, is possible, but less likely.

Once bound to their host, 10-15 mites mate on the surface of the skin.

Clinical manifestations

l Intense itching especially at night.

l Erythematous papules, excoriations and occasionally vesicles.

l Interdigital web spaces, wrists, axillary folds, periumbilical skin, pelvic girdle, penis and ankles.

l Classic linear burrows.

NORWEGIAN SCABIES

Norwegian scabies, caused by the ectoparasite Sarcoptes scabiei is a variant of classical scabies which is considered to be one of the most debilitating skin infestation. This mite infection is characterized by its specificity for compromised immune system-bearing population like patients with Human Immunodeficiency Virus (HIV) – Acquired Immunodeficiency Syndrome (AIDS), lymphomas, cognitive impaired and people on immunosuppressing medications. Unlike classical scabies, Norwegian scabies presents thick, exuding hyperkeratotic crusts with less or no itching. Patients having HIV infection are very prone to Norwegian scabies infection and the co-infection of HIV virus and Sarcoptes in patients is frequently reported (Maguire, 1960). More caution is warranted in such cases as Norwegian scabies in homeless AIDS patients is reported to have atypical presentation in a number of cases apart from the typical lesions (Schlesinger, 1994) which can lead to a delayed diagnosis or misdiagnosis of the infection resulting in increased chances of its transmission in the institutions connected with the patients.

Norwegian scabies in homeless AIDS patients present the clinical manifestations including hyperkeratosis in soles and palms and thickening of nails. This non-pruritic infection comes as lesions on the shoulders, back, elbows and thighs in the infected individuals (Sirera, 1990). The skin scrapings from these regions are first clinically examined to confirm the presence of mites before commencing a line of treatment for such patients. AIDS patients with Norwegian scabies pose a big risk of not only transmitting this highly contagious dermatological problem, but also of getting a secondary opportunistic infection.

Diagnosis

l Clinical presentation.

l Skin scraping and demonstration of the mite microscopically.

Complications

l Secondary impetiginization.

l Eczematous eruption.

l Scabies incognito if corticosteroids are used.

l Delayed hypersensitivity reaction.

Prevention

l Gloves.

l Prophylactic treatment for close contacts.

l Isolation and the use of disposable items.

Treatment

l 1% solution of Lindane not for infants, pregnant women or after a bath.

l 5 % cream Permethrin safer.

l 6% – 10% precipitated sulfur in petrolium daily for 3 days.

l Antipruritic drugs.

l Treat secondary infections.

l Ivermectin in severe cases.

l Treat all contacts and linen.

References

1. Chosidow O. Clinical practice. Scabies. N Engl J Med. 2006 Apr 20;354(16): 1718–27.

2.Dupuy A, Dehen L, Bourrat E, et al. Accuracy of standard dermoscopy for diagnosing scabies. J Am Acad Dermatol. 2007 Jan;56(1):53–62.

3.Walter B, Heukelbach J, Fengler G, et al. Comparison of dermoscopy, skin scraping, and the adhesive tape test for the diagnosis of scabies in a resourcepoor setting. Arch Dermatol. 2011 Apr;147(4):468–73.

4.Albrecht J, Bigby M. Testing a test: critical appraisal of tests for diagnosing scabies. Arch Dermatol. 2011 Apr;147(4):494–7.

5.Scabies fact sheet. Atlanta: Centers for Disease Control and Prevention, 2005. Available at: http://www.cdc.gov/ncidod/dpd/parasites/scabies/factsht_scabies.htm. Accessed: December 15, 2011.

PTHIRUS PUBIS

1. http://animaldiversity.ummz.umich.edu/accounts/Pthirus_pubis/

2. http://www.youtube.com/watch?v=TaCWT0HK_KA

l Crab louse.

l Could be found other than genital region.

l 2mm in length, powerful legs, hair attachment, moves slowly.

l Incomplete metamorphosis, eggs, nymph and adult.

l Eggs operculated, shiny, stick to hair (nits)

Clinical manifestations

l Pruritis.

l Maculopapular rash.

l Excoriation.

l Eye lashes scaling.

l Skin thickening, macular swellings, hyperpigmentations, Subcutaneous hemorrages (Vagabond’s disease).

Diagnosis

l Clinical manifestation.

l Nits, nymphs or adult louse.

Treatment

Treatment Safety profile/use Efficacy

Resistance of insect to treatment

1.0.33% pyrethrins + PBO shampoo

2.1% to 5% permethrin cream rinse

3.1% creme rinse, wash off after 10 min.

4.1% lindane lotion and shampoo

5.Ivermectin 0.8 % shampoo

l Lindane.

l Permethrin.

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l Antipruritic drugs.

http://video.about.com/dermatology/Treating-Head-Lice.htm

References

1. Roberts, L., J. Janovy. 2000. Foundations of Parasitology 2nd ed.. McGraw-Hill Higher Education.

2. Flinders DC, DeSchweinitz P. Pediculosis and scabies. Am. Fam. Phys. 2004;69:341–348.

3. Bignell C. Lice and scabies. Medicine. 2005;33:76–77.

4. 4. Diaz JH. The epidemiology, Diagnosis, Management, and prevention of Ectoparasitic diseases in travelers. J. Trav. Med. 2006;13:100–111.

5. 19. Davidson JK, Moore NB, Earle JR, Davis R. Sexual attitudes and behavior at four universities: do region, race, and/or religion matter? Adolescence. 2008;43:189–220. [PubMed]

6. 21. Lichtenstein B. The stigma of sexually transmitted infections: Knowledge, Attitudes, and an educationally-based intervention. Health Educ. Monogr. ser. 2008;25:28–33.

Family: Demodicidae Demodex folliculorum (human hair follicle mite)

1. http://emedicine.medscape.com/article/1203895-overview#a0104

2. http://www.youtube.com/watch?v=_AQYpxLYvto

Pathophysiology

D folliculorum (all stages) is found in small hair follicles and eyelash hair follicles. In all forms, immature and adult, it consumes epithelial cells, produces follicular distention and hyperplasia, and increases keratinization leading (in eyelashes) to cuffing, which consists of keratin and lipid moieties. Demodex brevis (all stages) is present in the eyelash sebaceous glands, small hair sebaceous glands, and lobules of the meibomian glands. Adults and immature forms consume the gland cells in all of these loci and, when infestations are heavy, can affect the formation of the superficial lipid layer of the tear film coacervate. Demodectic mites produce histologically observable tissue and inflammatory changes, epithelial hyperplasia, and follicular plugging.

Infestation of the eyelash hair follicle results in easier epilation and more brittle cilia. These mites also serve as vectors of infective elements and interrupt tissue integrity. They have been implicated in meibomian granulomas and are associated with certain dermatologic changes. All reported histologic sections of lid follicles infested with D folliculorum show distention and thickening. Coston claims that less than one half of the specimens he observed showed perifollicular lymphocytic infiltration.

Follicular inflammation produces edema and results in easier epilation of the eyelashes. It also affects cilia construction, and lashes are observed to be more brittle in the presence of demodicosis. Madarosis (loss of lashes) is associated with abundant mites, the loss of eyelashes as a result of intercellular edema in the hair shaft, and loss of hair resiliency. Although epithelial hyperplasia associated with follicular plugging is often encountered, dermal changes seldom extend beyond the perifollicular epidermal area. Once believed to be mite excreta, this plugging is now known to be epithelial hyperplasia with interspersed layers of lipid. The formation of a collar of tissue around the base of the lashes is observed clinically. This occurs significantly more often in follicles infected with D folliculorum. The epithelial hyperplasia is hypothesized to be most likely a product of the abrasive action of the mite’s claws.

Accumulation of waste material of the follicle mite may occur in affected follicles or sebaceous glands. Electron micrographs of the mite surface and feces show bacterial, viral, and rickettsial elements. Specific reports have revealed that both species pierce epithelial cells and consume cytoplasm. Only D brevis has been observed with channels burrowed to the germinal epithelium in the sebaceous glands.

Demodex species-induced pathologic changes have been implicated in dry eye conditions. When follicular plugging involves the meibomian gland (D brevis) or the gland of Zeis (D folliculorum or D brevis), reduction of the superficial lipid layer of the tear film occurs. The effect of D brevis on the meibomian structure has been implicated in chalazion formation. Chalazia are granulomatous inflammation of the meibomian glands, made of an organized core of epithelioid cells and histocytes surrounded by fibroblasts, lymphocytes, and plasma cells. These defense cells encircle particles too large for normal macrophages to engulf. D brevis has been observed in the center of these meibomian granulomas. Lid infestation by the Demodex species may or may not accompany dermatologic changes of the nose, the cheek, or the forehead.

D folliculorum has been suggested as a factor in pityriasis folliculorum. This dermal inflammation manifests itself as a diffuse erythema of the affected areas; scaly, dry skin; and, in certain cases, rosacealike lesions. The dry skin cycle described by Ayres is initiated when the demodectic mite plugs the follicle and reduces the sebaceous outflow, which leads to scaling as well as rough and dry skin texture.Sebaceous outflow is further reduced when patients inadvertently decide to apply facial cream. The mite flourishes in this environment of oily additives, leading to an increase in the population of the mites and a continuation of the dry skin cycle.

Clinical Presentation

Symptoms

Ocular irritation
Itching
Scaling of lids
Gross observation

Lid thickening
Scaling of lids
Madarosis (loss of lashes)
Conjunctival inflammation
Meibomian gland dysfunction
Rosacea
Decreased vision

Slit lamp findings

Collar of tissue around the base of the eyelashes
Follicular distention
Dry eye
Cornea

Superficial corneal vascularization
Marginal corneal infiltration
Phlyctenule-like lesion
Superficial corneal opacity
Nodular corneal scar

Causes

Demodex species specific to humans occupy 2 periocular sites hidden from external observation. They are small in size and possess the ability to move across the skin surface.
D folliculorum is found in hair and eyelash follicles associated with pilosebaceous glands in the eye or elsewhere on the face and the body. A single follicle may contain as many as 25 D folliculorum organisms.
D brevis leads a much more solitary lifestyle in sebaceous glands of the body and in the meibomian gland and the gland of Zeis.
D folliculorum measures 0.3-0.4 mm in length, whereas D brevis is one half the size of D folliculorum (0.15-0.2 mm) with similar structure of the head and the thorax but a shorter abdomen.
The 8 legs of this arachnid are segmented and provide locomotion at a rate of 8-16 mm/h.
D folliculorum and D brevis, also known as follicle mites, are believed to be more active in the dark, although capture in daylight is possible.
The bright light of the day and especially the biomicroscope cause the mite to recede back into the follicle. Therefore, the mite can be observed only when an epilated lash is observed under a low-power microscope.
The life stages of D folliculorum begin with copulation at the mouth of the follicle. Reproduction is believed to occur in darkness; a fact that is significant in symptomatology and treatment.
Following copulation, the female burrows back into the follicle near the opening of the pilosebaceous gland and lays her eggs.
Spickett reported the life cycle of D folliculorum and estimated that only 14.5 days elapse from ovum to adult stage, including 120 hours as an adult. Females may live an additional 5 days after oviposition.
Sexes are separate; sexual maturity is reached in the larval form (neoteny).
Females are territorial; they remain in their respective follicles and wait for the nomadic philandering males that travel over the surface of the skin from one follicle to another in seek of females.
Adults reside in the follicle parallel to the hair shaft, head inward, often with the tail end (opisthosoma) protruding onto the surface of the skin at the base of the eyelash.

Differential Diagnoses

Imaging Studies

By visualizing the metazoan parasite under high-power magnification, a definitive diagnosis can be made.
An epilated lash examined under low-power magnification may demonstrate the organism.
Adding a fluorescein solution after mounting further helps in detecting and counting the mites that are embedded in cylindrical dandruff of epilated eyelashes.
Electron microscopy has been used to visualize the organism.

Demodex folliculorum

Demodex brevis

Histologic Findings

All reported histologic sections of lid follicles infested with D folliculorum show distention and thickening. Coston claims that less than half the specimens he observed showed perifollicular lymphocytic infiltration.Follicular inflammation produces edema and results in easier epilation of the eyelashes. It also affects cilia construction, and the lashes are observed to be more brittle in the presence of demodicosis. Dermal changes seldom extend beyond the perifollicular epidermal area, although epithelial hyperplasia associated with follicular plugging is often encountered.

Eyelid section shows Demodex folliculorum (M) in the hair follicle.

Section of sebaceous gland of an eyelash shows Demodex brevis (M).

Cross-section through small hair follicle of the eyelid.

Medical Care

The treatment regimen is divided into in-office care and at-home care.

In the office, D folliculorum can be lured to the follicle surface with the use of volatile fluids, such as ether (not allowed in the United States), brushed vigorously across the external lid margin, following 0.5% proparacaine instillation. Five minutes later, a solution of 70% alcohol is applied in a similar manner. This regimen is reported to successfully reduce both the symptoms and the observed number of mites by the end of 3 weekly visits. Ether and alcohol should be used with caution, and corneal contact should be prevented.
A combination of this in-office treatment with a home regimen is suggested. The home regimen includes scrubbing the eyelids twice daily with baby shampoo diluted with water to yield a 50% dilution and applying an antibiotic ointment at night until resolution of symptoms.
Various treatments have been used to control Demodex mites. Most treatments involve spreading an ointment at the base of the eyelashes at night to trap mites as they emerge from their burrow and/or move from one follicle to another.

Mercury oxide 1% ointment is frequently used.
Pilocarpine gel reduced the number of mites and alleviated the symptom of itching in 11 patients in a nursing home. Celerio et al hypothesized that pilocarpine was directly toxic to the mites because its muscarinic action impedes respiration and motility.

The latest popular treatment regimen includes the use of 50% tea tree oil with Macadamia nut oil, applied with cotton tip applicators, after one drop of tetracaine.

Aggressively debride the lashes and the lash roots first with scrubs. Try to get the oil into the lash roots and along the lashes to kill any eggs. Treat the eyebrows as well. Three applications, 10 minutes apart, per visit are recommended; treatment is completed with compounded 20% tea tree ointment. Repeat for 3 visits, each one week apart.
Home regimen includes the following:

Use tea tree shampoo on hair and eye lashes every day.
Use tea tree soap or face wash every day.
Buy new makeup and discard old makeup; do not use makeup for 1 week.
Clean sheets and buy new pillows.
Check spouse; if both have this problem, both need to be treated.
Check pets.
For the first few weeks, use the ointment at night after tea tree shampoo scrubs. If inflammation is present, combination steroid-antibiotic ointments may be applied for one week. This is then replaced with a pure antibiotic ointment or with compounded 10% tea tree ointment.

References

1. Morfin Maciel BM. [Demodicidosis in a female patient treated as allergic blepharoconjunctivitis. A case report]. Rev Alerg Mex. Nov-Dec 2003;50(6):232-6. [Medline].

2.Morrás PG, Santos SP, Imedio IL, Echeverría ML, Hermosa JM. Rosacea-like demodicidosis in an immunocompromised child. Pediatr Dermatol. Jan-Feb 2003;20(1):28-30. [Medline].

. Karincaoglu Y, Bayram N, Aycan O. The clinical importance of demodex folliculorum presenting with nonspecific facial signs and symptoms. J Dermatol. Aug 2004;31(8):618-26. [Medline].

4.Kheirkhah A, Casas V, Li W, Raju VK, Tseng SC. Corneal manifestations of ocular demodex infestation. Am J Ophthalmol. May 2007;143(5):743-749. [Medline].

5.Lacey N, Kavanagh K, Tseng SC. Under the lash: Demodex mites in human diseases. Biochem (Lond). Aug 1 2009;31(4):2-6. [Medline]. [Full Text].