Praise Allah SWT who has given grace and His gift to us so that we can complete the tutorial

report titled Module 1 red spots on the skin.

This report contains questions and answers and an explanation of the module 1. Our berarap
what we have discussed together from tutorial 1 and 2 can we learn well and can we apply.

This report may be very far from perfection, but we are looking forward to feedback and
criticism in making the report.

end I said thank you profusely to mentor and also to all those who helped in the completion of
this report. may be useful for us and

Makassar, 14 July 2015

 BAB I
PREFACE

The skin covers the entire external surface of the human body and is the principal site of
interaction with the surrounding world. It serves as a protective barrier that prevents internal
tissues from exposure to trauma, ultraviolet (UV) radiation, temperature extremes, toxins, and
bacteria. Other important functions include sensory perception, immunological surveillance,
thermoregulation, and control of insensible fluid loss.

Skin also varies in thickness among anatomic location, sex, and age of the individual. This
varying thickness primarily represents a difference in dermal thickness, as epidermal thickness is
rather constant throughout life and from one anatomic location to another. Skin is thickest on the
palms and soles of the feet (1.5 mm thick), while the thinnest skin is found on the eyelids and in
the postauricular region (0.05 mm thick).

Because the skin is an organ located at the outside it is very vulnerable to diseases, one of which
is derived from the word comes dermatitis.DermatitisDerm / o (skin) and itis (inflammation /
inflammation) so that dermatitis can be translated as a condition in which the skin is inflamed or
inflammation.
 BAB II
CONTENTS

red spots on the skin

scenario

A housewife was 20 years old come to the doctor with a private practice complaint demarcated
reddish spots on wrist, appeared 4 days ago. These spots is rather warm in touch, itchy, and there
is no pain in emphasis. The disorder is recurrent in nature, especially washing. Location disorder
can be in between fingers or toes interrupted

Difficult words:

1. Reddish spots : limited areas with discoloration.

2. Pain : sensation that make discomfort and make hurts.
3. Itch : sensation that make desire to scratch the itchy area.

Key words:

1. Housewife

2. Appears 4days ago

3. reddish spots on wrist

4. warm in touch, itchy, and there is no pain in emphasis

5. Location disorder can be in between fingers or toes interrupted

Question:

1. How is the anatomy of skin?

2. How about the histology and physiology of skin?

3. How is patomechanism of reddish spots?

4. How is the etiology of Tinea Pedis?

5. Explain the types of hypersensitivity!

6. Explain the correlation between the symptoms and washing!

7. explain the steps diagnosis!

 8. Explain the examination that we have to take to get diagnose!

Answer:

1. ANATOMY OF SKIN.
The skin is the largest organ of the body, with a total area of about 20 square feet. The
skin protects us from microbes and the elements, helps regulate body temperature, and
permits the sensations of touch, heat, and cold.
skin has three layers:
The epidermis, the outermost layer of skin, provides a waterproof barrier and creates our
skin tone.
The dermis, beneath the epidermis, contains tough connective tissue, hair follicles, and
sweat glands.
The deeper subcutaneous tissue (hypodermis) is made of fat and connective tissue.
The skin is a vital organ that covers the entire outside of the body, forming a protective
barrier against pathogens and injuries from the environment. The skin is the body's
largest organ; covering the entire outside of the body, it is about 2 mm thick and weighs
approximately six pounds. It shields the body against heat, light, injury, and infection.
The skin also helps regulate body temperature, gathers sensory information from the
environment, stores water, fat, and vitamin D, and plays a role in the immune system
protecting us from disease.

2.
HISTOLOGY AND PHYSIOLOGY OF SKIN
 Skin Histology

Epidermis layer
The epidermis consists of five layers:
1. Stratum corneum: squamous cell has no nucleus, protoplasm turned into keratin. Can not
be seen with the naked eye. keratinization (stratum corneum)
Stratum corneum (horny layer) is the most outer layer of skin and composed of several
layers of flattened cells that die, not core, and the protoplasm have turned into keratin
(horn substances).
2. Stratum lusidium
 2-3 Layer = Gepeng not nucleated cells
 Changes in Protein = protoplasm Eleidin
 Obviously on the palms and soles of the feet
Stratum lusidum are directly under koneum layer, a layer of flattened cells without
nuclei with protoplasm is transformed into proteins called eleidin. The layers appear
more clearly in the palms of the hands and feet.
3. Stratum granulosum
• 2-3 layers of flattened cells
• cytoplasmic granules, there are core comprises à keratohyalin
Granular layer (layer keratohialin) is 2 or 3 layers of flattened cells with coarse grained
cytoplasm and nucleus in between. These coarse grains consist of keratohialin. Mucosa
usually do not have this layer. Granular layer is also evident in the palms of the hands and
feet.
4. Stratum spinosum
• Form polygonal: different sizes
• The process of mitosis
Spinosum stratum (stratum Malphigi) or also called prickle cell layer, consists of
several layers of cells are shaped polygonal different magnitude because of the process of
mitosis. The protoplasm looks clear because many contain glycogen, and core located in
the middle. These cells are closer to the surface more and more flattened shape.
5. Stratum basale
 Shaped palisade
 basal cells = mitosis and reproductive function
 Layer 2 consists of:
1. columnar cells
2. Melanocytes = clear cell: cell light-colored, basophilic cytoplasm and the nucleus dark
and have melanosomes
Epidermis: no blood and lymph vessels

II. Dermis Layer

Elastic and fibrous layer with cellular elements and the hair follicle consists of two parts:
A. Pars papillare = protruding into the epidermis
      contains blood vessels and nerve vessels
B.Parsretikulare = protruding into subcutaneous, thicker and connective tissue

III. Subcutaneous layer

1. The skin glands consist of:
 sudorifera glands (sweat glands): eccrine glands, apocrine glands
 sebaceous glands (glands Pallid)
2. Hair
3. Nails
4. Muscle

Skin Physiology

Skin can easily be seen and touched, live, and ensure viability. Supports the skin's
appearance and personality. Thus, the human skin has a very important role, in addition
to the primary function of ensuring the survival also has another meaning that is
aesthetic, race, systemic indicator, and non-verbal means of communication between
individuals on one another.
The main function of the skin is protection, absorption, excretion, perception, regulation
of body temperature (thermoregulation), the formation of pigment, mechanical formation,
such as pressure, friction, attraction; chemical disturbance, such as chemical substances
of vitamin D, and keratinization.
1. The function of protection.
Skin protect the inside of the body to injury or physical things that irritants, such lisol,
carbolic acid and other strong alkali and interruption that hot, for example radiation,
shock, ultraviolet light. Outside interference, especially bacterial infections or bacteria or
fungi. This is possible because of the fat pads, thick layer of skin and supporting tissue
fibers that act as a protective physical disorders.
Melanocytes continue to play a role in protecting the skin against sun exposure to provide
protection tanning chemical stimuli can occur due to the nature of the stratum corneum is
impermeable towards various chemicals and water, in addition to which there is a layer of
skin that protects the acidity of the chemicals contact with skin. The acidity of the skin
layer may be formed from the sweat and sebum excretion, the acidity of the skin causing
skin pH range of pH 5 to 6.5 so that a chemical protection against bacterial and fungal
infections. Keratinization process also acts as a barrier (barrier) mechanical die because
the cells break away regularly.
2. The absorption
Healthy skin is not easy to absorb water, solution and solid, but volatile liquid is more
easily absorbed as fat soluble. Skin permeability to O2, CO2, and water vapor allows the
skin took part in respiratory function. Absorptive capacity of the skin affected by the
thickness of the skin, hydration, moisture, metabolism and type vehikulum. Absorption
can take place through the gaps between cells, penetrate the epidermal cells or through
the mouth of the gland duct; but more of the cells of the epidermis through a gland
3. The function of excretion
 Skin glands release substances that are no longer useful or metabolic waste in the body,
such as NaCl, urea, and ammonia. Oil glands on the effect of androgen hormones fetus
from the mother produces sebum, to protect the skin against the amniotic fluid, at birth
found in vernixcaseosa. Sebum is produced to protect the skin's sebum as well as oiling
of the skin also withstand excessive water evaporation resulting in dry skin. Product
sweat and oil glands in the skin causing skin acidity of pH 5 to 6.5.
4. The perception
Skin contains sensory nerve endings in the dermis and subcutaneous. The heat stimulus
was played by agencies in the dermis and subcutaneous Ruffini. The cold played by
bodies located in the dermis Krause. Meissner tactile body is located in the dermal papilla
contributes to the touch, as well as body Merkel Ranvier, located in the epidermis. While
the pressure played by Maccinivater body in the epidermis. Sensory nerves are more
numerous in the erotic.
 5. Function settings
The skin did the body temperature (thermoregulation) role with sweat and wrinkled
(muscle contraction) the blood vessels of the skin. Skin rich in blood vessels that allow
the skin to get enough good nutrition. Vascular tone is influenced by the sympathetic
nervous (acetylcholine). In infants usually blood vessel walls not yet fully formed,
causing extravasation of fluid because the baby looks more edematous skin because it
contains a lot of water and Na.
6. The formation of pigment
Melanocytes located in the basal layer and cells derived from neural ridge. Comparison
of basal cell counts; melanocytes is 10: 1. Melanocytes and the large number of pigment
granules (melanosomast) determines skin color, race or individual. He outward
appearance of these cells in the clear round and a dendrite cells, called pla as clear cell.
Melanosum formed by the Golgi apparatus with the help of the enzyme tyrosinase, Cu
and O2. Exposure to sunlight affects the production of melanosum. Dispersed pigment
epidermis through the hands of dendrite while the skin layer underneath taken by cell
melanofa (melanoform). Skin color is not completely affected by skin pigment, but also
the thickness of the skin, reduction of hemoglobin, oxy-H and carotene.
7. The keratinasi
Adult epidedrmis layer has three main types of cells keratinocytes, Langerhans cells,
melanocytes. Starting with basal cell keratinocytes entered fission, the other basal cells
will move up and metamorphose into a cell on the cell spinosum become progressively
more and more depressed and granular to granular cells. The longer the core is removed
and keratinocyte cell horn became amorphous. This process is ongoing lifetime, and until
 now has not been fully understood. Matoltsy believes may keratinocytes through the
process of synthesis and degradation into the stratum corneum. This process normally
lasts for about 14-21 days, the skin and provides protection against infection is
mechanically and physiologically.
7.Theformation of vitamin D
This function is made possible by changing 7 dihydroxy cholesterol with the help of
sunlight. But the necessities of life will not be enough vitamin D just from that, so that
systemic administration of vitamin D is still needed. In human skin, can also express
emotions because their blood vessels, sweat glands, and the muscles under the skin.

3. PATOMECHANISM OF REDDISH SPOT

After a single exposure or repeated exposure to the same agent. Patomekanisme red
spots, namely: First, the chemicals damage the dermal cells directly with direct
absorption across the cell membrane and then damage the cell system. The second
mechanism, after the cell is damaged, it will stimulate the release of inflammatory
mediators to the region by T cells and mast cells are non-specific, for example, stimulate
the release of arachidonic acid and phospholipids by phospholipase assistance.
Arachidonic acid is then converted by the cyclooxygenase (produces prostaglandins,
thromboxane) and lipoosigenase (produce leukotrienes). Prostaglandins can cause
dilation of blood vessels (so it looks red).

4. ETIOLOGY OF TINEA PEDIS

Tineapedis

Athlete's foot (tineapedis) is a fungal infection of the skin of the foot. Most athlete's foot
is caused by one of two types of fungus.

 Trichophytonmentagrophytes often causes toe web or vesicular (blisterlike) infections.

The infection appears suddenly, is severe, and is easily treated.
 Trichophytonrubrum often causes moccasin-type infections. This condition lasts for a
long time (chronic) and is difficult to treat.

You get athlete's foot when you come in contact with the fungus and it begins to grow on
your skin. Fungi commonly grow on or in the top layer of human skin and may or may
not cause infections. Fungi grow best in warm, moist areas, such as the area between the
toes.
 Athlete's foot is easily spread (contagious). You can get it by touching the affected area
of a person who has it. More commonly, you pick up the fungi from damp, contaminated
surfaces, such as the floors in public showers or locker rooms.

Although athlete's foot is contagious, some people are more likely to get it (susceptible)
than others. Susceptibility may increase with age. Experts don't know why some people
are more likely to get it. After you have had athlete's foot, you are more likely to get it
again.

If you come in contact with the fungi that cause athlete's foot, you can spread the fungi to
others, whether you get the infection or not

A dermatophyte infection of the feet most commonly caused by Trichophytonrubrum,

less commonly caused by T. interdigitalis and E. floccosum.

5. TYPES OF HYPERSENSITIVITY
A. Type 1 : Anaphylactic hypersensitivity

There are 3 phase allergen come into our body that makes immune response like IgE production
of allergy :

1. Sensitasion phase
Time which needed to make IgE until cross binding by specific receptor in this case is FCR at the
surface of mast cell.
2. Activation phase
Time which needed to re-display with specific antigen and mast cell/basofil will released its
contents which contain granule to make a reaction. It can be happened by cross bond among
antigen and IgE.
3. Effector phase
When the response / complex (anaphylaxis) as an effect ofmediators which releases by mast cell
or basofil with farmacologic activity. In this case, the farmacologic active (amin vasoactive) by
mast cell and basophil, all of that’s mediators make contraction of smooth muscle, increasing
vascular permeability and vasodilatation, and also tissues damage and anafilactid.

Type 1 allergic disease, often referred to as atopic disease, is a group of condition occurring in
people with a hereditary predisposition to produce immunoglobulin E (IgE) antibodies against
common environmental antigens (allergens).These condition include some of the commonest
cause or ill health including allergic rhinitis, asthma, and atopic eczema.

Type 1 allergic reaction are due to activation of Th2 and the overproduction of IgE
antibodies.

The reason for this overproduction of IgE antibodies in certain individuals is unclear. There is
increasing evidence that lack of exposure to bacteria which stimulate TH1 responses in early life
favors the Th2 phenotype with subsequent development of atopy. This “hygiene hypothesis”
could explain the lower incidence of allergic disease in individuals who farm or live in rural
communities where they are presumably exposed to organisms form livestock. Allergic reactions
are initiated by a limited number of allergens which are deposited in low doses on mucosa,
epithelium or skin. This is a particularly efficient way of activating Th2 cells and inducing IgE
responses. Allergic individuals not only have larger numbers of allergen specific Th2 cells in
their blood, but these cells produce greater amounts of interleukin-4 (IL-4) per cell than Th2 cells
from normal people. As with other antigens, allergens are processed by Langerhans or other
antigen presenting cells and are proteolytically cleaved into small peptides and presented to
uncommitted Th0 cells. In the case of an allergic response, these cells now differentiate into Th2
lymphocytes, which release various cytokines that inhibit Th1 cell activation and upregulate IgE
production. These cytokines, particularly IL-4 and IL-13 together with signals delivered by the B-
cell surface molecule CD40, induce isotype switching in newly generated IgM bearing-cells from
μ to ∈ resulting in subsequent of IgE.

There is a strong genetic component to allergic disease.

Genetic susceptibility to allergic reactions has not been clearly defined but high levels of IgE are
noted in certain allergic (atopic) families. Human leukocyte antigen (HLA) linkage is associated
with allergic responses to a number of allergens including ragweed and house dust mite. A further
major genetic locus, which regulates serum igE levels, has been identified on chromosome 5q in
the region containing the genes for IL-4, IL-5, and IL-9, cytokines that are important in regulating
IgE synthesis. Polymorphism of the IL-9 gene is associated with asthma, as is a locus on
chromosome 11q12 where the gene encodes the β chain of the IgE receptor.

Clustering of IgE receptors on mast cells trough cross linking triggers anaphylaxis

Mast cells display a high affinity receptor (FcεRI ¿for the Cε 2 :Cε 3 junction region of IgE Fc, a
property shared with their circulating counterpart, the basophil. Cross linking of receptor bound
of IgE antibodies by a multivalent antigen will trigger release of the inflammatory mediators
responsible for the acute allergic reaction through aggregation of these receptors. Activation is
rapidly followed by the breakdown of phosphatidylynosiiol to inositol triphosphate (IP3), the
generation of diacylglycerol (DAG) and an increase cascade allows the granules to fuse with the
 plasma membrane and release their preformed mediators into the surrounding tissue. It also
results in synthesis of lipid mediators including a series of arachidonic acid metabolites formed
by the cyclooxygenase and lipoxygenase pathways, and production of a variety of cytokines
which are responsible for the late phase of the acute allergic reaction.

Mast cell and basophil mediators

Mast cell degranulation is the major initiating event of the acute allergic reaction. The preformed
mediators released from the granules include histamine, heparin, tryptase, neutral protease in
various eosinophil and neutrophil chemotactic factors. Histamine itself is responsible for many of
the immediate symptoms of allergic reaction including bronchoconstriction, vasodilatation,
mucus secretion and edema caused by leakage of plasma protein from small vessels. These
effects can all be reproduced and visualized in the immediate skin test where allergen injected
into the skin produces a characteristic wheal and flare reaction with redness, edema and pruritus
(itchiness). Tryptase released by mast cells activates receptors on endothelial cells that selectively
attract eosinophil and basophil.

Activation of the mast cell also results in the liberation of newly formed lipid mediators, which
include the leukotrienes LTB4, LTC4,LTD4, the prostaglandin D2 , PGD2, and Platelet activating
factor (PAF). Prostaglandin D2, the leukotrienes and PAF are highly potent bronchoconstrictors,
which also increase vascular permeability and are chemotactic for inflammatory cells.

The late phase of the allergic reaction is mediated by cytokines

Mast cells and basophils are responsible for significant production of proinflammatory cytokines
including to more necrosis factor (TNF), IL-1, IL-4, and IL-5 and chemokines such as MIP-1 α
and MIP1 β . Within 12h of an acute allergic reaction a late-phase reaction occurs which is
characterized by a cellular infiltrate of CD4+ cells, monocytes and eosinophil. These cells will
themselves release of variety of Th2-type cytokines, especially IL-4, and IL-5, which are
responsible for further inflammation and the site of allergen.

B. Type II. Antibody dependent cytotoxic hypersensitivity

It happened because there is antibody like IgG or Ig M to the antigen which is the past of host
cell. Firstly there is a reaction between antibody and determinant of antigen which is the past of
membrane depend with complement or accessory molecul and metabolism cell.

Cytolitic exactly remembered the reaction that happend because lysis and not the effect of toxic.
That Antibodi can activation the cell who has FCγ −R receptors, and also NK Cell which lead as
an efector cell and can make damage through ADCC (Antibody Dependent Cell (mediated )
cytotoxic.

 This involves the death of cells bearing antibody attached to a surface antigen.
 The cells may be taken up by phagocytic cells to which they adhere through their coating of IgG
or C3b, or they may be lysed by the operation of the full complement system.
 Cells bearing IgG may also be killed by polymorphsand monocytes or by natural killer (NK) –
cells through the extracellular mechanism of antibody dependent cellular cytotoxicity (AADC).
 Examples are : Transfussion reaction, hemolytic disease of the newborn through rhesus (Rh)
incompatibility, antibody mediated graft destruction, autoiimmune reaction directe against the
formed elements of the blood and kidney glomerular basement membranes, and hypersensitivity
resulting from the coating of erythrocyte or platelets by a drug.

C. Type III Hypersensitivity reactions

In the normal condition immune complex in the sirculation is bound and transported by
eritrocyte to liver, limph, and damaged by mononuclear fagocyte cell, such as in the liver,
limph, lung without complement help. The general big complex can be easy and fast to
be damaged by macrofage in the liver. Small and soluble complex is difficult to be
damaged, therefore it can be more long time in the sirculation. Probably fagocyte
function obstruction is one of causing why complex is difficult to be damaged. The
problem will arise if immune compex settle in the tissue.

1. immune complex settled in the blood vessel

immune complex consist of antigen in the sirculation and IgM or IgG3 (or IgA) are
settled in the vascular basal membrane and kidney basal nembrane that cause local and
big inflamation reaction. Complex that occurs can cause trombocyte agregation,
macrofage activation, mast cell activation.

2. immune complex settled in the tissue

it allows the deposition of immunee complexes occur in the tissue is a measure of
immunee complexes that is small and vascular permeability increased , partly because the
histamine is released by mast cell.

3. Reaction form
a) Local reaction or phenomenon Arthus
Arthus horse serum is injected intradermally into rabbits in the same place repeatedly
finding increasingly intensified reactions at the injection site.
Arthus type reactions may occur intrapulmoner induced germs, mold spores or dried fecal
protein that can cause pneumonitis or alveolitis or Farmer's lung.
C3a and C5a (anaphylatoxin) formed on the activation of complement, increasing the
permeability of blood vessels that can lead to edema. C3a and C5a also functions as a
chemotactic factor ,. Neutrophils and platelets begin to be deployed in the reaction and
menimbullkan static and total obstruction of blood flow. Anaphylatoxin target is the
small blood vessels, mast cells, smooth muscle, and peripheral leukocytes that cause
smooth muscle contraction, mast cell degranulation, increased vascular permeability and
triple response against the skin. Neutrophils were activated immunee complexes
consuming and together with the coagulated platelets release a variety of materials such
 as proteases, olagenase and vasoactive materials. Finally bleeding accompanied by local
tissue necrosis.
b) Type III systemic reactions - serum sickness
Type III systemic reactions so often seen in the administration of antitoxin serum
containing foreign origin such as tetanus or antidifteri horses.

Antibodies whose role is usually the type of IgM or IgG . Anafiltoksin release
diaktifan complement ( C3a , C5a ) that stimulate mast cells and basophils release
histamine . Other mediators and MCF ( C3a , C5a , C5 , C6 , C7 ) mobilize
polymorphs which release proteolytic enzymes and proteins polycationic . immunee
complexes are easier to deposited in places with elevated blood pressure and current
lap accompanied , for example in the glomerular capillary , bifurcation of blood
vessels,the choroid plexus and ciliary body of the eye .

Complement also cause the aggregation of platelets that form microthrombi and
release of vasoactive amines .

D. Type IV hypersensitivity reaction

Type IV hypersensitivity reaction is granulomatosis . there are several phases in response
that begins with a type IV sensitization vase that require 1-2 weeks after the primary
contacts with antigen . in that phase , Th activated by the APC although MHC - II .
Typical DTH reaction as other immune responses , such as the phase of sensitization and
effector phase

Clinic manifestation

a. Contact dermatitis
Contact dermatitis is CD4+ desease that can occur contact with undangerous thing, such
as DTH reaction. Contact with thing such as formaldehyde and nicle.

b. Tuberculin hypersensitivity
The important role in this reaction is CD4+ T lymphocyte cell. After injecting tuberculin
extract intracutan, red area in the injection area on 12-24 hours.

c. Jones Mote reaction

Jones Mote reaction is type IV hypersensitivity to protein antigen that has relation with
basophil infiltration on the skin under of dermis. Another type IV hypersensitivity, this
reaction is weak.

d. T cell mediated cytolysis ( penyakit CD8+)

 In the T Cell mediated cytolysis, damaging occurs although CD8+ that directly kill target
cell

6. CORRELATION BETWEEN SYMPTOMS AND WASHING.

Some materials that contained in detergent are alkalis. Such as:

-active materials, sodium lauryl sulfonate. It can caused iritan on epiderm and
denaturation polipeptide cycle of protein molecule, which is can make the structure of
protein cycles are changed.

-additional materials, such as Na2CO3. It can make hot effect for our skin.

-parfume materials, like alcyl benzena sulfonate. Can cause dermatitis contact, because
water are hipotonic, so it makes skin erosion.

Dermatitis Contact

Dermatitis that caused by substances or materials that exist in our skin. Divided into two.
They are:- alergic dermatitis contact

- irritant dermatitis contact

Alergic Dermatitis Contact

Alergic responses that appear when we have contact with alergen materials.The main
poin is, parfume materials can caused alergic dermatitis contact.

Factors That Involved Dermatitis:

1. Temperature

2. Age

3. Gender

4. History of Desease

5. Personal Hygiene

7. DIAGNOSE STEPS
for diagnosis:
1. anamnesis
Questions asked include: detailed history of exposure to possible allergens, frequency,
duration, intensity, location and development of symptoms related to the determination of
the probable cause and a decision on the type of therapy that may be effective. It should
also be asked about family history of close, because allergies can be familial.
2. Physical examination
-Whole skins must be considered whether there is chronic inflammation such as
scratches, there are lesions and dematitis.
-inspeksi, palpation, percussion and auscultation
Other proofing in the form of low blood pressure often found in people with allergies.

But allergens cause an allergic response is not fully known from the history and
examination of the symptoms. However, when the certainty of the results of the
investigation have not felt stronger then investigations should be carried out. There are
two ways of doing investigations or allergy tests are in vitro and in vivo.

3.Support examination
 Skin Prick Test (SPT)
The substance suspected allergen is placed on areas of the skin, usually on the inside of
the forearm, upper arm or back of the hand. Tested allergen extracts can be more than one
so that the skin of the hands can be marked in such a way to test as well. Extracts of
allergens presented at the skin with a distance of 3 cm between allergens and at least 2
cm from the elbow. Then the superficial layer of skin pierced with a special lancet needle
(long needle eye 2 mm) so that the allergen can penetrate the skin but not to cause
bleeding wounds. Changes in the skin, such as swollen and red, and then monitored after
15-30 minutes (rapid test) .If appear allergic response in the form of lesions with a
diameter> 2 mm then the result is positive.

 Test Scratch / Scratch Test

Is used to determine how the response is generated after the skin exposed to allergens.
Allergens is contacted to the skin for 48 hours and at a time to see how the new 72-96
hours response resulting in skin. This method has been widely abandoned because less
accurate.
 Test Paste / Patch Test
Used to determine allergic contact dermatitis chemicals in diseases and eczema. The
substance is suspected allergen is placed on the back skin. If the result is positive, the
response in the form of red spots will appear within 48-72 hours after exposure (slow
response) .condition to perform this test within 48 hours of the patient is not allowed to
move that up to sweat, bathe, sleep face down (the back of the inevitable friction). 2 days
 before testing, pasein not allowed to consume drugs containing steroids (anti-swelling)
and back area must be free of topical drugs.

8. EXAMINATION TO DIAGNOSE
 Irritant Contact Dermatitis
Irritant contact dermatitis is an inflamation of skin caused by non-immunological skin
contact with that are irritants physically can damage skin, such as acid, alkali and the
others
Patophysiology:
On irritant contact dermatitis skin damage occurs without any prior allergic reaction.
Keratinocyte membrane damage activates phospolipase then form AA(arakidonic acid),
DAG( diasilgliserida), IP3( inositides), PAF(platelet activatic factor). AA wil turn into
PGS( prostaglandins) and LTS ( leukotrienes). DAG and IP3 would influence the
formation of proteins that lead to the emergence of IL-1( Interleukin-1) and GM-CSF
( Granulocyte Macrophage Colony Stimulatin Factor). IL-1 will active T helper
lymphocyte cells that eventually form IL-2 and the IL-2 receptor on the cell surface of T
lymphocites. This process will eventually stimulate keratinocytes to proliferate and as
we all know will keratynocyte produce ICAM-1 (Intra Celullar Adhesion Molecule),
PGs and LTs are as chemoattractant that attract cells of neutrophils and lymphocytes and
also activate mast cell to form histamine. LTs, PGS, PAF that will cause changes in the
blood vessels. The onset of this inflamation we known as irritant contact dermatitis.
Clinical sign
Generally, patients complains itch. Skin disorders depending on the severity of
dermatitis. Acute condition began with erythema patches bounded clear, then followed
edema, papulovesicle, vesicles or bulla. When vessicles or bullae rupture it can lead to
erosion and exudation (wet). Meanwhile, on the cronic condition skin looks scaly,
papules lichenification may also fissure and there isnt clear boundaries.
Diagnostic:
Diagnosis is based on the results of acurrate anamnesis and thorough clinical
examination. Subject areas according to the type of materials or substnces with regard to
the skin directly like hands and toes. On the clincal examination there are lymphocyte
transformation test, magrophage migration inhibition test and patch test
Treatment:
1. Give a suggestion toa wear protector like hand gloves if the patient’s always touch
chemical substance like a farmer
2. Give kortikostroidsistemic drugs: oral and topical
3. If there is a secondary infection give antibiotic
  ALLERGIC CONTACT DERMATITIS

Allergic contact dermatitis is a common skin condition which causes an itchy and
weeping rash localised to the area in contact with the allergic trigger (allergen). It usually
develops two or more days after contact with the allergen. It lasts as long as contact
continues and for a short time (typically 1 to 2 weeks) afterwards.

Allergic contact dermatitis occurs when a substance to which you're sensitive (allergen)
triggers an immune reaction in your skin. It usually affects only the area that came into
contact with the allergen. But it may be triggered by something that enters your body
through foods, flavorings, medicine, or medical or dental procedures (systemic contact
dermatitis).

You may become sensitized to a strong allergen such as poison ivy after a single
exposure. Weaker allergens may require multiple exposures over several years to trigger
an allergy. Once you develop an allergy to a substance, even a small amount of it can
cause a reaction.

Common allergens include:

 Nickel, which is used in jewelry, buckles and many other items

 Medications, such as antibiotic creams and oral antihistamines
 Balsam of Peru, which is used in many products, such as perfumes, cosmetics, mouth
rinses and flavorings
 Formaldehyde, which is in adhesives, solvents and other things
 Personal care products, such as deodorants, body washes, hair dyes, cosmetics, nail
polish, and herbal preparations for the skin containing eucalyptus, camphor or rosemary
 Skin tattooing and black henna
 Plants such as poison ivy and mango, which contain a highly allergenic substance called
urushiol
 Airborne substances, such as from aromatherapy and spray insecticides
 Products that cause a reaction when you're in the sun (photoallergic contact dermatitis),
such as some sunscreens and oral medications

The rate of allergic contact dermatitis in children is similar to that in adults. Children
develop the condition from the usual offenders and also from exposure to car seats, the
plastic in toilet seats and infant clothing snaps.
 ALLERGIC CONTACT DERMATITIS TREATMENT & MEDICATION

Topical corticosteroids are the mainstay of treatment, while a variety of symptomatic

treatments can provide short-term relief of pruritus. However, the definitive treatment of
allergic contact dermatitis is the identification and removal of any potential causal agents;
otherwise, the patient is at increased risk for chronic or recurrent dermatitis. Online
resources allow the physician to create a list of products free of allergens to which the
patient is allergic.

The goal of pharmacotherapy is to reduce morbidity and to prevent complications.

Topical glucocorticosteroids are the mainstay of therapy. Topical calcineurin inhibitors
(immunomodulators) may be preferred for persistent facial particularly periocular
dermatitis. When choosing a topical glucocorticosteroid, match the potency to the
location of the dermatitis and the vehicle to the morphology (ointment for dry scaling
lesions; lotion or cream for weeping areas of dermatitis).

For severe acute allergic contact dermatitis (eg, poison ivy dermatitis, erythroderma),
systemic glucocorticosteroids or other immunosuppressive medications (eg, azathioprine)
may be occasionally needed for widespread and severe chronic dermatitis, particularly to
airborne allergens such as feverfew (Parthenium hysterophores).

In some cases, allergic contact dermatitis may prove persistent despite avoidance of the
allergen. In some of these cases (eg, nickel), ingestion of minute amounts of the allergen
is believed to drive the process, and chelation therapy with disulfiram can be beneficial.
In other instances, the cause of persistence remains enigmatic; many allergens penetrate
through rubber gloves. Psoralen–ultraviolet A (PUVA) therapy can be helpful in these
cases.

Oral antihistamines may help diminish pruritus caused by allergic contact dermatitis.

Diagnostic studies for allergic contact dermatitis include the following:

 Potassium hydroxide preparation and/or fungal culture: To exclude tinea; these tests are
often indicated for dermatitis of the hands and feet
 Patch testing: To identify external chemicals to which the person is allergic
 Repeat open application test (ROAT): To determine whether a reaction is significant in
individuals who develop weak or 1+ positive reactions to a chemical
 Dimethylgloxime test: To determine whether a metallic object contains enough nickel to
provoke allergic dermatitis
 Skin biopsy: May help to exclude other disorders, particularly tinea, psoriasis, and
cutaneous lymphoma
 The definitive treatment for allergic contact dermatitis is the identification and removal of
any potential causal agents; otherwise, the patient is at increased risk for chronic or
recurrent dermatitis. Treatments also include the following:

 Corticosteroids: Topical corticosteroids are the mainstay of treatment, although acute,

severe allergic contact dermatitis, such as from poison ivy, often needs to be treated with
a 2-week course of systemic corticosteroids
 Topical immunomodulators (TIMs): Approved for atopic dermatitis, but they are also
prescribed for cases of allergic contact dermatitis when they offer safety advantages over
topical corticosteroids
 Phototherapy: Administered to individuals with chronic allergic contact dermatitis that is
not controlled well by topical corticosteroids; these patients may benefit from treatment
with a combination of psoralen (a photosensitizer) and ultraviolet-A (PUVA)
 Immunosuppressive agents: Chronic immunosuppressive agents are, in rare instances,
used to treat recalcitrant cases of severe, chronic, widespread allergic contact dermatitis
or severe hand dermatitis that prevents a patient from working or performing daily
activities

Disulfiram: Occasionally, an individual who is highly allergic to nickel and has severe
vesicular hand dermatitis will benefit from treatment with disulfiram (Antabuse); the
drug has a chelating effect

 DERMATOMYCOSES

Definition:

A dermatomycosis is a highly contagious skin disease caused by fungi. It affects both

people and animals. Other names of dermatomycosis are tinea, ringworm, jock itch, and
athlete’s foot. There are three groups of fungi that can cause dermatomycosis:

- Anthrophilic fungi use human as their primary reservoir.

- Geophilic fungi live in the soil and cause ringworm in people and animals.
- Zoophilic fungi live on animals other than people, but can be transferred to people.

We will deal only with zoophilic fungi that are transmitted from animals to people.

Etiology :
Two genera of zoophilic fungi, Microsporum and Trichophyton, are responsible for
nearly all cases of dermatomycosis that are zoonotic. The spore of these fungi are able to
survive in the environment, is protected areas, for 18 months or more. They rely on
keratid, a protein found in the outer layer of the akin, hair, feathers. Nails, and hoovers,
for survival. They thrive when on a person or animal, on shed hair, or on dead skin cels.

Transmission

Not every person or animal that comes in contact with these fungi will develop clinical
disease. Some animals or people will be carriers while remaining asymptomatic. Young
animal and children are most often affected because their immune systems are not fully
developed. The same is true for people with suppressed immune systems such as people
with HIV/AIDS, those receiving chemotherapy, and organt transplant recipient.

Dermatomycosis in Humans

Tinea corporis is seen on the skin. The lesions appear as small, red spots that grow into
large rings on the arms, legs or chest.

Etiology
Trichophyton
Microsporum
Epidermophyton

Tinea pedis is also known as athlete’s foot. The lesion usually begin between the toes,
where the skin is moist. They become red and itchy and have a wet surface. If the fungus
spreads to the toenails, it become Tinea ungulum. The toenails become thick and crumby,
scratching the area can spread the infection to hands and fingernails.
 Etiology:

T.rubrum, T.mentag, E.floccosum

Tinea cruris, also known as jock itch, is caused by fungus growing in the moist, warm
area of the groin. The lesions are found most often in men who frequently wear athletic
equipment.

Etiology : E. floccosum, T. rubrum, T. mentagrophytes

Tinea capitis, also known ringworm, is found on the head. The lesions begin as itchy,
red areas where eventually hair is destroyed, leaving bald patches. Ringworm is the most
common dermatomycosis in children.

Etiology : Trichophyton, Microsporum

 Diagnose

Beyond the clinical signs, there are three methods used to diagnose dermatomycosis:

 The Woods Lamp is a special blacklight that emits filtered ultraviolet light. When
exposed to a woods lamp, many but not all fungi will fluoresce bright blue green. A lack
of fluorescence doesn’t indicate that no fungus is present. Dander and certain topical
medications will also fluoresce.

 Hair is pulled from the outer edges of the lesion, where the fungi are still active. The
hairs are placed on a microscope slide in a KOH (Potassium hydroxide) solution to make
the spores more visibe. They are then examined under a microscope for the presence of
spores on the hair shaft. This method of diagnosis is useful up to 70% of the time.
 For identification if the spesific fungus causing the dermatomycosis, hair from the edge
of the lesion must be cultured on specializedmedia in a specific environtment. Growth
can take up to several weeks, and each fungus grows uniquely appearing colonies on the
media.

Treatment

 Both topical and oral medications are available, some of them over the counter
 Topical medications include creams, ointments, sprays, shampoos, and dips.
 Anyone who has had to suffer the smell of lime sulohur dip for treatment of ringworm in
a cattery knows that prevention is much better than treatment.
 Treatment may last a long time, even after the person or animal appears better. The
fungus can remain even after the hair has grown back.

Prognose

The prognosis is Fausta, ifchroniccanbedubiousandFausta.

Daftar pustaka:

1. Buku ilmu penyakit kulit dan kelamin, Ed.V 2010 FKUI

2. Journal emedicine.medscape.com
3. Daniel J, Hogan. “Allergic Contact Dermatitis”.12 Juli 2015.
http://emedicine.medscape.com
4. American College of allergy, asthma, & immunology. “Contact Dermatitis”. 12 Juli
2015. http://acaai.org/allergies/types/skin-allergies/contact-dermatitis

5. Imunologi dasar. Edisi 11 cetakan ke-2. Hal : 333-344

6. Essential immunology Roitts.10th Editon.2010.USA:Black Well Publishing.p322-323
7. Karnen Garna Bratawidjaja.2006.Imunologi Dasar . Edisi 7.Jakarta :Balai Penerbit FKUI
8. Ilmu Penyakit Kulit dan Kelamin Edisi V Fakultas Kedokteran Universitas Indonesia