LAPORAN KELOMPOK 8 PBL

MODUL 2
“RED SPOT ON SKIN”
BLOK TROPIS

Tutor : dr. Irmayanti HB, Sp.PK

By :
Group 8

11020170083 Hasri Ainun Basri

11020170084 Nurul Fitriana Ibrahim
11120170085 Muh. Akram Mu’fid
11020170086 Aulia Chaeruni
11020170087 Kasma
11020170089 Yasmin Fadhilah Ardiyati
11020170090 Aulia Putri Salsabila Burhan
11020170092 Elfatri
11020170093 Putri Saskia Aulyah NR
11020170094 Melinia Fajri Ramadhani

FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR

2019

pg. 1
Scenario 2
A woman came to the health center with complaints of itching on the
body, under the folds of the breast and around the buttocks since 1 month ago.
Initially appeared little by little, accompanied by reddish color, shape like a
prickly heat, felt rather wet. Because itching is very annoying, because it often
scratches into wounds, feels sore and the color becomes blackish. Itching is
especially felt when sweating. There is no history of allergies. This itching had
improved after being given a hydrocortisone ointment, but in this week the itching
on the body even more widespread until the stomach and back are increasingly
blacked color with a rough feeling on the skin.
A. DIFFICULT WORD
Nothing.
B. KEYWORD
1. A woman
2. Itching on the body, under the folds of the breast and around the buttocks
since 1 month ago
3. Reddish color, shape like a prickly heat, felt rather wet
4. Feels sore and the color becomes blackish
5. There is no history of allergies
6. Itching when sweating
7. Itching had improved after being given a hydrocortisone ointment
8. Itching more widespread until the stomach and back
C. QUESTIONS
1. Whats the etiology of red spot ?
2. Any disease that causes red spot on skin ?
3. Why itching felt more when sweating ?
4. Why itching complaints are felt under the folds of the breast and the
buttock ?
5. Why complaints widespread and blackened color after being given a
hydrocortisone ointment ?
6. Explain the diagnostic step according to the scenario ?

pg. 2
 7. Whats the differential diagnose of the scenario ?
8. Whats the first treatment of the scenario ?
9. Explain perspective islam!

D. ANSWER

1. Whats the etiology of red spot

1. Allergens: drugs, food, dust, temperature, etc.

Histamine release factor to activate basophil through increased IgE.
So patients who are hypersensitive to food and are exposed to producing
cytokine antigens (histamine release factors) interactions with IgE will
bind to the surface of the basophils and cause the release of histamine.
The inflammatory process occurs when the histamine mediator is
released when antigens enter a specific area of the skin. Locally, released
histamine will cause vasodilation which induces redness and increased
capillary permeability as a result, so that within a few minutes there will
be swelling in the clearly demarcated area.
2. Infection: viruses, bacteria, fungi, and other types of microbes and
parasites.
Red spots can be caused by infectious agents such as viruses. The
virus that enters our body at first has not been recognized by our immune
system so that this virus can escape and live latently and spread to
sensory nerves to the ganglion (sacral). If there is a trigger factor, this
virus will produce cytokines, namely TNFα and IL-1 and IL-8 as
proinflammatory cytokines. This viral toxin will stimulate the production
of TNFα so that IL-1 causes adhesion and leukocytes in the endothelium
and secretes protease and arachidonic metabolites. This activates the
clotting system so that the body compensates by increasing [ermebaility
(vasodilation). But because this virus is fast replication and is supported
by trigger factors so that the lesions caused are also not offset by platelet
factors so that blood seeps into the skin of the dermis and epidermis
causing red spots.

pg. 3
3. Viruses: HSV-1, HSV-2
4. Mushrooms: Epidermophyton Floccosum, Tinea Rubrum,
Trichophyton Mentagrophytes.
5. Trauma
The occurrence of skin neglect in atopic dermatitis is also determined
by the presence of trauma to the skin. Mechanical trauma to keratinocytes
causes the release of cytokines that can induce inflammation through the
release of IL-1, TNFα and IL-4. These cytokines subsequently induce
adhesion molecules (ex : ELAM-1, ICAM-1, and VCAM-1) which cause
lymphocytes, macrophages, and eosinophils to enter skin inflammation.

ANATOMY
The skin is an elastic wrapper that protects the body from
environmental influences. The skin is also the heaviest and widest
body tool, which is 15% of body weight and an area of 1.50 - 1.75
m. Average thickness of skin 1-2 mm. The thickest (6 mm) is in
the palms and legs and the thinnest (0.5 mm) is in the penis. The
skin is divided into three main layers, namely the epidermis,
dermis or corium, and subcutaneous or subcutaneous tissue.1

i
Picture1. Skin of Anatomy

pg. 4
a. Epidermis, divided into four layers, namely:
1. Basal layer or Stratum Germinativum
2. Malpighi or Stratum Spinosum layer
3. Granular layer or Sratum Granulosum
4. Layer of the Horn or Stratum Corneum

On the palms and feet there is an additional layer above the

granular layer, namely Stratum Lusidium or clear layers. Stratum
Lusidium, the cells are flat, the difference with the stratum
granulosum is that many cells have lost the nucleus and cell grains
have become clear and very clear. translucent. In layers it looks
like a clear band, cell boundaries are not so visible, called stratum
lusidium.1

The basal layer or germinativum, is called the basal stratum

because the cells are located in the basal part. The stratum
germinativum replaces the cells that are above and are stem cells.
The shape is cylindrical (tube) with an oval core. Inside there are
fine grains called color melanin grains. The cells are arranged like
a fence (palisade) at the bottom of the cell there is a membrane
called the basement membrane. Basal cells with basement
membrane are the lowest boundary of the epidermis with the
dermis.1

The Malpighi or spinosum / akantosum layer, this layer is the

thickest layer and can reach 0.2 mm consisting of 5-8 layers. The
cells are called spinosum because if we look under the microscope
the cells consist of cells that are polygonal in shape (many angles)
and have horns (spina). It is called Akantosum because its cells are
thorny. It turns out that the spina or horn is a connection between
other cells called Interceluler Bridges or intercellular bridges.

pg. 5
Granular layer or stratum granulosum, this stratum consists of flat
cells such as coils. These cells are only 2-3 layers parallel to the
surface of the skin. In the cytoplasm there are grains called
keratohiolin which are phases in the formation of keratin because
of the many stratum granulosum grains. The stratum corneum, the
cell is dead, has no cell nucleus (the cell nucleus is dead) and
contains keratin.1

The epidermis also contains eccrine glands, apocrine glands,

sebaceous glands, hair and nails. Sweat glands are of two types,
eccrine and apocrine. Its function is to regulate body temperature,
causing heat to be released by evaporation. Eccrine glands are
found in all areas of the skin, but not in the mucous membranes.
They number between 2 and 5 million, the most in the palm. The
secretions are clear liquid, about 99% containing chloride, lactic
acid, nitrogen, and other substances. The apocrine gland is a large
sweat gland that empties into the hair follicles. in the armpits,
anogenital area, nipples, and areola.1

Sebaceous glands are found throughout the body, except in the

palms, soles, and instepes. There are many scalp, face, forehead,
and chin. The secretions are sebum and contain fatty acids,
cholesterol, and other substances. Hair is found throughout the
body, hair grows from hair follicles in the epidermis. Hair follicles
are limited by the upper epidermis, basically there is papil where
the hair grows.1

b. Dermis
The dermis is the second layer of the skin. The boundary with
the epidermis is covered by the basement membrane and in the
lower border is the subcutis but this limit is not clear. The dermis

pg. 6
consists of two layers, namely the upper part, the papillary pars
(stratum papilar) and the lower part, the reticular (stratum
reticular).1

The boundary between the papillary pars and the reticular pars
is the lower part to the subcutis. Both the papillary pars and the
reticular pars consist of loose connective tissue composed of fibers
namely collagen fibers, elastic fibers and reticulus fibers1

c. Subcutis
Subcutis consists of collections of fat cells and between these
groups travel fibers of the dermis connective tissue. These fat cells
are round in shape with their core being pushed to the side, so they
form like a ring. This layer of fat is called the adiposus peniculus
whose thickness is not the same in each place and also the division
between men and women is not the same (different). Adiposus
peniculus is a shock braker or spring when mechanical trauma
stresses on the skin, heat insulation or to maintain temperature,
accumulation of calories, and add to body beauty. Under the
subcurtis there is a muscular membrane and then there is muscle.1

PHYSIOLOGY
The skin is the most extensive surface organ that encloses the
entire outside of the body so that the skin as a body protector
against the dangers of chemicals, sunlight contains ultraviolet light
and protects against microorganisms and maintain the body's
balance to the environment. The skin is an indicator for someone to
get a general impression by seeing the changes that occur in the
skin. For example, becoming pale, yellowish, reddish-red or
increased skin temperature, showing abnormalities that occur in the
body skin disorders due to certain diseases.1

pg. 7
Skin Function
Skin in humans has a very important function besides
establishing survival in general, namely:
1. Protection
The skin protects the inside of the body against physical or
mechanical disorders, for example against friction, traction,
chemical disturbances that can cause irritation (lisol, carbolic acid
and strong acids). Heat disorders such as radiation, ultraviolet
light, interference from infections such as bacteria and fungi.
Because of the presence of fat pads, the thick layers of skin and
supporting tissue fibers act as protectors against physical disorders.
Melanocytes play a role in protecting the skin against sunlight by
holding tanning (treatment with acetyl acid).1
2. Protection of chemical stimuli
Can occur due to the nature of the stratum corneum which is
impermeable to various chemicals and water. In addition there is a
layer of skin acidity that protects the contact of chemicals with the
skin. The acidity layer of the skin is formed from the results of
sweat and sebum excretion which causes skin acidity between pH
5-6.5. This is protection against fungal infections and dead skin
cells break away regularly.1
3. Absorption
Healthy skin does not easily absorb water, solvents and solid
objects, but volatile liquids are more easily absorbed, so are those
that dissolve in fat. Skin permeability to O2, CO2 and water vapor
allows the skin to take part in the function of respiration. The
ability of skin absorption is influenced by the thickness of the skin,
hydration, moisture and metabolism. Absorption can take place
through gaps between cells, penetrate epidermal cells, or through
glandular channels and more through epidermal cells.1

pg. 8
4. Heat Regulator
Body temperature remains stable despite changes in
environmental temperature. This is because there is an adjustment
between the heat generated by the central heat regulator, medulla
oblongata. Normal body temperature is visceral temperature 36-
37.5 degrees for lower skin temperatures. Nerve and vasomotor
control of arterial cutaneous are two ways namely vasodilation
(capillaries widen, the skin becomes hot and excess heat is emitted
into the sweat glands so that there is evaporation of fluids on the
surface of the body) and vasoconstriction (blood vessels constrict,
the skin becomes pale and cold, the loss of sweat is restricted and
excess heat is emitted into the sweat glands resulting in
evaporation of fluids on the surface of the body) and
vasoconstriction (blood vessels constrict, skin becomes pale and
cold, sweat loss is limited , and body temperature heat is not
released).1
5. Excretion
Skin glands secrete substances that are no longer useful or
metabolic waste in the body in the form of NaCl, urea, uric acid,
and ammonia. Sebum produced by the skin is useful for protecting
the skin because the layer of sebum (an oily substance that protects
the skin) retains excessive water so the skin does not become dry.
The production of fat and sweat glands causes acidity in the skin.1
6. Perception
The skin contains sensory nerve endings in the dermis and
subcutis. The response to heat stimulation is played by the dermis
and subcutis, to the cold played by the dermis, civilization is
played by the dermis papillae and the renvier markel, while the
pressure is played by the epidermis. Sensory nerve fibers are more
numerous in erotic areas.1

pg. 9
7. Pigment Formation
Pigment formation cells (melanocytes) are located in the basal
layer and these cells originate from nerve rigi. Melanocytes form
skin color. Melanosum enzymes formed by golgi tools with the
help of tyrosinase, Cu ions, and O2 to sunlight affect melanosum.
Pigment is spread to the epidermis through the dendritic hands
while the underlying layer is carried by melanofag. Skin color is
not always influenced by skin pigment but also by the thickness of
the skin, reduction in Hb and carotene.1
8. Keratinization
Keratinocytes are started from basal cells that hold division.
Other basal cells will move up and change into spinous cells. The
more up this cell, the more flattened and granular into granulosum
cells. The longer the core disappears and these keratinocytes
become amorphous horn cells. This process continues for a
lifetime. Keratinocytes go through a process of synthasis and
degeneration into a layer of horns that lasts approximately 14-21
days and provide skin protection against infection through
physiological mechanisms.1
9. Formation of vitamin D
By changing cholesterol dehydroxy with sunlight help. But the
need for vitamin D is not enough just from the process. Provision
of systemic vitamin D is still needed.1

HISTOLOGY
The skin is tissue that covers the surface of the body, which
consists of 2 layers:
1. An epithelium called the epidermis
2. The binding tissue called the dermis or corium Epidermis
originates from the ectoderm and the dermis originates from the
mesoderm.

pg. 10
 Picture 2. Histology of skin

Based on morphological features and epidermal thickness, the

skin is divided into:
1. Thick skin
This thick skin is found in the man's vola and planta pedis
which do not have hair follicles. On the surface of the skin a
prominent line is called the crista cutis which is separated by
grooves called the sulcus cutis.2
EPIDERMIS
In the epidermis there are two systems
1. Malpighi system, part of the epidermis whose cells will undergo
keratinization.2
2. The pigmentation system, which is derived from the neural
crista and will provide melanocytes for the synthesis of melanin.
Besides cells - cells that belong to these two systems, there are
other cells, namely Langerhans cells and Markel cells whose
function is unclear.2

pg. 11
 Histological structure:
In the epidermis can be distinguished 5 strata, namely:

p
Picture 3. Epidermis of skin

a. Stratum basale
This layer is also called the stratum pigmentosum or strarum
germinativum because most mitotic cells are present. These lining
cells are bordered by corium binding tissue and are cylindrical or
cuboidal in shape. Inside the cytoplasm are pigment grains.2

b. Stratum spinosum
This layer together with the stratum basale is also called
stratum malpighi or stratum germinativum because the cells show
mitotic cells. The cells of the stratum basale will push the cells
above it and turn into polyhedrals. Stratum spinosum consists of
several layers of cells - shaped polyhedral and on examination with
a light microscope at the edge of the cell shows protuberances like
thorns. At first the projections were thought to be intercellular
bridges with tonofibrils connecting from one cell to another.2

pg. 12
 c. Stratum granulosum
This layer consists of 2-4 cells that are thick above the stratum
spinosum. Cell form like a rhombus that extends parallel to the
surface. The innermost cell is shaped like a cell in the strarum
spinosum only contains grains inside it. Items containing
cytoplasm are more colorful with hematoxylin (keratohialin grains)
which can be confused with pigments.2

d. Stratum Lucidum
It appears as a clear wavy line between the stratum granulosum
and the stratum corneum. Consists of several layers of cells that
have been flattened arranged very dense. This clear part contains
eleidin which is thought to be the result of keratohialin.2

e. Stratum Corneum
In the man's vola and planta pedis, this layer is very thick
which consists of numerous layers of flat cells which have
undergone cornification or keratinization. The connection between
cells as spines in the stratum spinosum is no longer visible. On the
surface, the layer will peel (desquamatio) sometimes - sometimes
referred to as stratum disjunctivum.2

2. Any disease that causes red spots on the skin?

a. Ptyriasis Rosea h. Dengue hemorrhagic fever

b. Herpes zooster i. Erythroderma
c. Candidiasis j. Scabies
d. Erythrasma k. Photosensitivity
e. Psoriasis l. Varicella
f. Contact dermatitis m. Tinea corporis
g. Urticaria n. Impetigo bullosa18

pg. 13
3. Why itching felt more when sweating ?

Histamine is an important mediator, not only as a cause of vasodilation,

protein secretion, and itching, but also directly triggers an inflammatory
response.13 Histamine is the most studied pruritogen at the moment. Besides
being stimulated by histamine can also be stimulated by temperature.14
The role of circulating immunoglobulins and slow type
hypersensitivity in the defense of the skin to deal with certain germs is still
largely unknown. IgM has never been found in sweat, and IgA, IgG, IgD are
only found in small amounts (0.01% of serum levels). However, the high
frequency of fungal infections specific to the skin and mucosa, suggests the
relationship with the immune response.13
Itching usually occurs in conditions of sweating and high temperatures,
as well as disappear and arise chronic. Some studies mention the
relationship between itching and sweating caused by increased sweat
production which will affect the occurrence of pruritus (especially in
patients with atopic dematitis). This is related to the role of acetylcholine in
the mechanism of itching induced by sweating. Repeated scratching away
from the location of the itching and heat stimulation of the nocsius inhibits
histamine-induced skin blood flow.15
Sweat occurs when the body's core temperature rises and spreads. To
reduce this and regulate body temperature, the body will increase blood
circulation to areas that are a source of heat. When it reaches a hot area, the
body gets confused and releases histamine to defend itself, because the body
feels that there will be health problems outside the body. The impact of this
release of histamine is itching. That is why the body feels itchy when
sweating. This is a temporary body reaction that can be lost.15

4. Why are itchy complaints felt under the folds of the breasts and
buttocks ?

pg. 14
 This can be caused by the folding of the breasts and thighs
which is the most closed part when a person is dressed. When the
ambient temperature is hot and someone sweats, fold the breasts
and thighs to be the most humid part due to sweat. This condition
supports the growth of the fungus candida in the groin and
eventually causes intertriginous candidosis. The second most
location is the armpit. Armpits are a part of skin that is moist
because it sweat a lot. The number of cases in the armpit location
is not as much as the breast and thigh fold because the armpits are
usually not covered with a tight cloth such as the breast and thigh
fold.
Most patients only have lesions at one skin fold location or two
skin fold sites infected with intertriginous candidosis. Only a few
patients are affected by more than two skin fold locations. This is
because the lesions on the skin in intertriginous candidosis patients
give itching, pain, and can even cause a burning sensation, so
patients tend to immediately seek help from the doctor before the
lesions spread to other skin folds.19

5. Why complaints widespread and blackened color after being given a

hydrocortisone ointment ?
Hydrocortisone is a type of corticosteroids that have anti-allergenic
and anti-inflammatory power. Corticosteroids work by preventing allergic
reactions, reducing inflammation, and inhibiting epidermal cells.
Hydrocortisone cream can reduce inflammation itching, and pain in the
skin. an indication of this cream, suppressing inflammatory reaction on
non-skinned skin 2-3 times a day. 10
The use of topical steroids on the skin due to fungal inflammation
can initially improve or decrease inflammation due to the main effect of
topical steroid administration on dermatology is the anti-inflammatory

pg. 15
 effect. But if treatment is stopped within a few days then the illness will
get worse and itchy. In addition to the anti-inflammatory effects of topical
steroids, they also have an immunosuppressive effect that suppresses
inflammation caused by fungi at the onset of infection, but if more and
more topical steroids are used, fungal infections will increase because
infectious organisms are not eradicated, but also topical steroids result in a
state of blurring. clinical infection so that it becomes unclear and
nonspecific. yeast infections given by a strong group of topical steroids
will make the lesions become reddish and gradually expand the infection.
This gives rise to an unclear and bizarre clinical picture of which squama
is almost absent, erythematous lesions with teleangiectasis which can also
include papules, pustules and hyperpigmentation.11

6. The steps to support the diagnoses

a. Anamnesis
b. Physical examination
c. Supporting investigation
a. Anamnesis
1. Patient identity : Name, age, address, job
2. Main complaint
Since when? Is the lessions persist? Where the lessions begin
to appearence? How it spread? Is the lesions increase or widened?
How is the color? Does it feel thick? Does it feel wet? What make it
worse? What make it better?
3. Accompanying complaint
Is there a fever? Is there a itching? Did before the lesions
appear there is an insect bite?
4. Past medical history
5. Family history
6. Contact with the same symptoms
7. Past therapy history

pg. 16
 8. Vaccination history
b. Physical Examination
1. General Condition
2. Nutrional Status
3. Vital Sign
4. Inspection
Location of lesions, the distribution, the size, the type of efflorescence
c. Supporting investigation
1. Patch testing
Patch testing is indicated when ACD is suspected and does not respond
to treatment, suggesting that the trigger has not been identified. In
patch testing, standard contact allergens are applied to the upper back
using adhesive-mounted patches containing minute amounts of
allergen or plastic chambers containing allergen held in place with
porous tape.
2. Biopsy
There are several types of skin biopsy:
1. Punch
2. Shave
3. Wedge excision
In a punch biopsy, a tubular punch (diameter usually 4 mm) is inserted
into deep dermal or subcutaneous tissue to obtain a specimen, which is
snipped off at its base. Shaving with a scalpel or razor blade may be
done for more superficial lesions. Bleeding is controlled by aluminum
chloride solution or electrodesiccation; large incisions are closed by
sutures. Wedge excision of skin using a scalpel can be done for larger
or deeper biopsies.Pigmented lesions are often excised for histologic
evaluation of depth; if too superficial, definitive diagnosis may be
impossible. Diagnosis and cure can often be achieved simultaneously
for most small tumors by complete excision that includes a small
border of normal skin.

pg. 17
3. Scrapings
Skin scrapings help diagnose fungal infections and scabies. For fungal
infection, scale is taken from the border of the lesion and placed onto a
microscope slide. Then a drop of 10 to 20% potassium hydroxide is
added. Hyphae, budding yeast, or both confirm the diagnosis of tinea
or candidiasis.For scabies, scrapings are taken from suspected burrows
and placed directly under a coverslip with mineral oil; findings of
mites, feces, or eggs confirm the diagnosis. However, a negative
scraping does not rule out scabies.
4. Examination by wood light
A Wood light (black light) can help clinicians diagnose and define the
extent of lesions (eg, borders of pigmented lesions before excision). It
can help distinguish hypopigmentation from depigmentation
(depigmentation of vitiligo fluoresces ivory-white and hypopigmented
lesions do not). Erythrasma fluoresces a characteristic bright orange-
red. Tinea capitis caused by Microsporum canis and M. audouinii
fluoresces a light, bright green. (Note: Most tinea capitis in the US is
caused by Trichophyton species, which do not fluoresce.) The earliest
clue to cutaneous Pseudomonas infection (eg, in burns) may be green
fluorescence
5. Tzanck testing
Tzanck testing can be used to diagnose viral disease, such as herpes
simplex and herpes zoster, and is done when active intact vesicles are
present. Tzanck testing cannot distinguish between herpes simplex and
herpes zoster infections. An intact blister is the preferred lesion for
examination. The blister roof is removed with a sharp blade, and the
base of the unroofed vesicle is scraped with a #15 scalpel blade. The
scrapings are transferred to a slide and stained with Wright stain or
Giemsa stain. Multinucleated giant cells are a sign of herpes infection.
6. Diascopy

pg. 18
 Diascopy is used to determine whether erythema in a lesion is due to
blood within superficial vessels (inflammatory or vascular lesions) or
is due to hemorrhage (petechiae or purpura). A microscope slide is
pressed against a lesion (diascopy) to see whether it blanches.
Hemorrhagic lesions do not blanch; inflammatory and vascular lesions
do. Diascopy can also help identify sarcoid skin lesions, which, when
tested, turn an apple jelly color.20

7. Whats the differential diagnose of the scenario ?

Candidiasis intertriginosa
Definition
Candidiasis is an acute or subacute skin disease, caused by an
intermediate fungus that attacks the skin, subcutaneous, mucous
membranes and internal organs.12
Etiology
The most common cause is Candida albicans which can be isolated
from the skin, mouth, vaginal mucous membranes, and feces of normal
people. As the cause of endocarditis candidiasis is C. parapsilosis and the
cause of systemic candidiasis is C. tropicalis.12
Epidemiology
Candidiasis found throughout the world can affect all ages both men
and women. The fungus is found in healthy people as saprophytes.
Clinical picture varies so that the data distribution is not known precisely.
This disease can be transmitted directly or indirectly. It is unclear where
the race is related to this disease but the incidence is thought to be higher
in developing countries. More in the tropics with high humidity.12
Classification
Based on the place affected by candidiasis classified in:
1. Candidiasis of mucous membranes
a. Thrush

pg. 19
 b. Perleche
c. Vulvovaginitis
d. Balanitis or balanopostitis
e. Chronic mucocutaneous candidiasis
f. Bronchopulmonary and pulmonary candidiasis
2. kandidiasis kutis
a. Local:
i. Intertriginous
ii. Perianal
b. General tourism
c. Paronychia and onychomycosis.
d. Granulomatous cutaneous candidiasis.
3. Systematic candidiasis
A. Endocarditis
b. Meningitis
c. Pyelonephritis
d. Septicemia
4. Reaction ID (Candidide)
Pathogenesis
Candida infection can occur if there are predisposing factors both
endogenous and exogenous12

a. Endogenous factors

Physiological changes
1. Pregnancy due to changes in pH in the vagina
2. Overweight, because a lot of sweat
3. Iatrogenic
4. Endocrinopathy, skin blood sugar disorders

pg. 20
5. Chronic disease: tuberculosis, lupus erythematosus with poor general
condition.
1) Age: parents and babies are more susceptible to infection because
their immunological status is not perfect.
2) Immunologic, genetic diseases

b. Exogenous factors
1. Climate, heat and humidity cause perspiration to increase
2. Skin hygiene
3. The habit of soaking feet in the air for too long causes maceration
and facilitates the entry of fungus
4. Contact with sufferers, for example in thrush, balanopostitis.

Clinical manifestations
Clinical manifestations of intertriginous candidiasis can be in the form
of lesions in the folds of the armpits of the skin, groin, intergluteal, breast
fold, between fingers or toes, glans penis, and umbilicus, in the form of
blotches that are firm, scaly, wet, and erythematous. The lesion is
surrounded by satellite lesions in the form of vesicles / pustules,
papulopustular or bullae which, when broken, leave an erosive area with
rough edges and develop like primary lesions. In chronic conditions, areas
are lichenification, hyperpigmentation, hyperkeratosis and sometimes
fistulas. Abnormalities in the skin cause severe itching complaints,
sometimes accompanied by burning and burning.12

Assistant Diagnosis
a. Direct Inspection

Skin scrapings or mucocutaneous smears are examined with a 10%

KOH solution or by Gram staining, visible yeast cells, blastospores, or
pseudohifa.12

pg. 21
 b. Culture Checks

The material to be examined is planted in Sabouraud glucose dextrose

agar, it can also be applied with antibiotics (chloramphenicol) to prevent
bacterial growth. Germination is stored at room temperature or cabinet
temperature of 370C, the colony grows after 24-48 hours, in the form of
yeast like colony. Candida albicans identification is done by breeding
these plants in corn meal agar.12
Diagnosis
The diagnosis is made on the basis of history, clinical manifestations,
physical examination and investigations.12
Differential diagnosis
Local cutaneous candidiasis with:
1. Erythrasma: folded lesions, redder lesions, firm boundaries, dry no
satellites, examination with brick red wood.
2. Dermatophytosis (tinea)
Management
1. Avoid or eliminate predisposing factors.
2. Topical:
a. Gentian purple solution ½-1% for membrane lenders, 1-2% for skin,
applied every day 2 times for 3 days.
b. Nystatin: contains creams, ointments, emulsions.
c. Amphotericin B
d Azol groups include:
1. Miconazole 2% contains cream or powder
2. Clotrimazole 1% consists of powder, solution and cream
3. Thioconazole, bufonazole, isoconazole
4. Cycloproxolamine 1% solution, cream
5. Other broad-spectrum antimycotics

3. Systemic:

pg. 22
 1. Nystatin tablets to eliminate gastrointestinal infections, these drugs
are not absorbed by the intestine
2. Amphotericin B is given intravenously for systemic candidiasis
3. For candidiasis vaginalis can be given cotrimazole 500 mg per
single dose vaginam, systemic can be given ketoconazole 2x200mg for
5 days or with itraconazole 2x200mg single dose or with fluconazole
150mg single dose
4. Itraconazole: if used for vulvovaginal candidiasis the dose for adults
is 2x100 mg daily, for 3 days
Prevention
a. Avoid or eliminate predisposing factors.
b. Maintain cleanliness.
c. Use clothing made from cotton which keeps conditions dry and air
circulation going well12
Prognosis
Generally good, depending on the severity of predisposing factors.12

Pediculosis Corporis
Definition
Skin infections caused by Pediculosis humanus var. corporis.9
Epidemiology
The disease usually affects adults, especially those with poor hygiene,
such as nomads, because they seldom bathe or rarely change and wash
clothes. Therefore, the disease is often called a vagabond disease. This is due
to lice do not cling to the skin, but the cotton fiber in the sea in between the
folds of clothes and only transient to the skin to suck blood. The spread of the
disease is cosmopolitan, more often in cold climates because people wear
thick clothes and rarely dicuci.9

Modes of Transmission
1. through clothing

pg. 23
2. In people with terminal hairy chest, this ticks can attach to the hair and can
be transmitted through direct contact

Etiology
Pediculosis humanus var. corporis have two sexes, the males and females,
the females a length of 1.2 to 4.2 cm and a width of approximately half its
length, while males are smaller. Life cycle through the stages of egg, larva,
nymph and mature9.

Pathogenesis
Skin disorders that arise due to scratching to relieve itching. The itching is
caused by the influence of saliva and excreta of fleas when sucking darah.9

Clinical symptoms
Generally only abnormality is found in the form of scratch marks on the
body, because new itch scratching decreases with more intensive. Sometimes
arise secondary infection with enlarged lymph nodes regional.9

Diagnosis
Finding lice and eggs on the cotton fibers clothes.9

Diagnosis differential
neurotic excoriation.9

Treatment
Treatment is with cream gameksan 1% were applied thinly throughout the
body and allowed to stand 24 hours, after which the patient a bath. If you still
have not healed repeated four days later. Other drugs are benzyl benzoate
25% emulsion and powder malathion 2%. Clothes to be washed with hot

pg. 24
water or ironed, for kill eggs dank utu. If there is a secondary infection treated
with antibiotics systematically and topical.9

Prognosis
Good to keep hiegene.9

Tinea Corporis

Definition
Tinea corporis is dermatophytosis in skin without hair (glabrous skin)
except for the palms, soles, and groins.
Dermatophytosis is a fungal infection caused by fungal dermatophytes
namely Epidermophyton, Mycrosporum and Trycophyton. There are more
than 40 different species of dermatophytes, which infect the skin and one of
the diseases caused by fungi is dermatophyte tinea corporis.6,7

Epidemiology
Tinea corporis is a common infection that is often seen in hot and humid
climates. Like other fungal infections, warm and humid conditions help
spread the infection. Therefore tropical regions and subtropics have a high
incidence of tinea corporis. Tinea corporis can occur at any age can be found
in workers associated with animals. Maceration and occlusion of the skin
folds cause an increase in skin temperature and moisture which facilitates
infection. Transmission can also occur through direct contact with infected
individuals or indirectly through objects that contain mold, eg towels,
bathroom floors, hotel beds, etc.6,7

Superficial fungal infection worldwide is estimated to affect 20-25% of the

world's population and is one of the most common forms of skin infection.
This disease is spread throughout the world that can attack all races and age
groups so that superficial fungal infections are relatively often affected in

pg. 25
 tropical countries (hot climate and high humidity) and frequent
exacerbations.6,7

Etiology and Pathophysiology

Dermatophytes are a class of fungi that cause dermatophytosis. This group of
fungi has keratin digesting properties. Dermatophytes belong to the class of
fungi imperfecti which are divided into three genera, namely Trichophyton
spp, Microsporum spp, and Epidermophyton spp. Although all dermatophytes
can cause corporate tinea, the most common causes are Trichophyton Rubrum
and Trichophyton Mentagrophytes. Dermatophyte infection involves 3 main
steps. The first attachment to keratinocytes, superficial fungi must pass through
various obstacles to be attached to the keratin tissue including UV light,
temperature, humidity, competition with other normal flora, sphingosin
produced by keratinocytes. And the fatty acids produced by the sebaceous
glands are fungistatic. The second penetration through or between cells, after
the spore attachment must develop and penetrate the stratum corneum at a
faster pace than the desquamation process. Penetration is also aided by the
secretion of proteinase lipase and mucinolytic enzymes which also provide
nutrients for fungi. Trauma and maceration also help the penetration of fungi
into the tissues. Fungal mannan in dermatophyte cell walls can also reduce the
rate of keratinocyte proliferation. New defenses emerge when once the fungus
reaches the innermost layer of the epidermis6,7
The final step in the development of the host response, the degree of
inflammation is influenced by the immune status of the patient and the
organism involved. Type IV hypersensitivity reactions (Delayed Type
Hypersensitivity (DHT) play a very important role in fighting against
dermatifita. In patients who have never been infected with dermatophytes
before inflammation causes minimal inflammation and the trichopitin test
results are negative. Infection results in slight erythema and squama resulting
from increased keratinocyte replacement. It is hypothesized that dermatophyte
antigens are processed by epidermal langerhans cells and presented by T

pg. 26
 lymphocytes in the lymph nodes. T lymphocytes proliferate and migrate to the
infected place to attack the fungus. At this time, the lesion suddenly becomes
inflamed and the epidermal barrier becomes permeable to transferrin and
migrating cells. Soon the fungus disappears and the lesion spontaneously
heals6,7

Clinical Features
Clinical features begin with round or oval lesions with active margins with
outward progression, patches may widen and eventually give a polycyclic,
arsinar and sirininar appearance. On the margins found active lesions that are
marked by erythema, the presence of papules or vesicles, while in the section
the middle of the lesion is relatively quieter. Chronic Tinea corporis, active
signs disappear and then only leave the hyperpigmentation area only. 6,7

Picture 4A. Picture 4B.

Tinea corporis usually occurs after contact with infected individuals or pets, but
sometimes occurs due to contact with wild mammals or contaminated soil. Spread
can also occur through objects such as clothing, furniture and so on.6,7

Laboratory Checks

pg. 27
 Aside from the typical symptoms of tinea corporis, the diagnosis must be
assisted with laboratory tests including microscopic examination, culture, wood
lamp examination, biopsy and histopathology, serological examination, and
examination using PCR (Hay and Moore, 2004).
Microscopic examination is done by making preparations directly from skin
scrapings, then the preparation is poured with 10% KOH solution. After 15
minutes or after being heated with low heat, viewed under a microscope. This
examination gave positive results of hyphae found hyphae (threads) that were
seeped or branched, in addition there were also spores in the form of small balls of
1-3μ.6,7
Culture was carried out in the media so that the patient was at room
temperature (25-300C), then one week was seen and assessed whether there was
mold growth. Fungal species can be determined through the form of colonies,
hyphae forms and spore forms.Wood lamp inspection is an examination using
ultraviolet light with a wavelength of 365 nm. This ray is not can be seen. When
this ray is directed at the skin that has been infected by certain dermatophyte
fungi, this ray will turn into visible by giving color (fluorescence). Some fungi
that give fluorescence are M.canis, M.audouini, M.ferrugineum and
T.schoenleinii.6,7

Comparative Diagnosis
There are several differential diagnoses of tinea corporis, including
erythema centrifugum erythema, numular eczema, granuloma anulare, psoriasis,
seborrheic dermatitis, pityriasis rosea, lichen planus and contact dermatitis.6,7

Diagnosis
Diagnosis is based on clinical symptoms and laboratory tests that are
direct microscopic and culture.6,7

Treatment

pg. 28
 Treatment of fungal infections can be divided into non-medical
treatment and medical treatment.

Non-medical
According to the Indonesian National Drug and Food Control Agency
(2011), it is said that the management of non-medical devices is as follows:
a. Use a separate towel to dry the affected part or the infected part is dried last to
prevent the spread of infection to other parts of the body.
b. Do not use towels, clothes, or other objects in turn with an infected person.
c. Wash towels and clothes contaminated with fungus with hot water to prevent
the spread of the fungus.
d. Clean the skin every day using soap and water to remove the remnants of dirt
so that fungus is not easy to grow.
e. If possible avoid the use of clothes and shoes that can cause skin to always get
wet such as wool and synthetic materials that can inhibit air circulation.
f. Before using shoes, you should first wipe and clean the dust from the shoes.
g. Avoid direct contact with people who have fungal infections. Use sandals made
of wood and rubber.6.7

Medical
Tinea corporis treatment consists of local and systemic medicine. In
tinea corporis with limited lesions, enough topical medication is given. Duration
of treatment varies between 1-4 weeks depending on the type of drug. Oral
medications or a combination of oral and topical medications are needed in large
or recurrent chronic lesions. Topical antifungal agents that can be given are
derivatives of imidazole, toxicic acid, haloprogin and tolnaftate. Local treatment
of fungal infections in inflamed lesions accompanied by vesicles and exudates is
first performed with an open wet compress.6,7
In a state of prominent inflammation and severe itching, the combination of
antifungals with short-term corticosteroids will accelerate clinical improvement
and reduce patient complaints.6,7

pg. 29
1. Topical Treatment
Topical treatment is the main choice. The effectiveness of topical drugs is
influenced by the mechanism of action, viscosity, hydrophobicity and acidity of
the formulation of the drug. In addition to classical drugs, imidazole and
allylamine derivate drugs can be used to overcome this problem of tinea corporis.
The effectiveness of the drug including the imidaol group more or less the same.
The administration of the drug is recommended for 3-4 weeks or until the culture
results are negative. Furthermore, it is also recommended to continue treatment
for 7-10 days after clinical and mycological healing with the intention of reducing
recurrence (Verma and Heffernan, 2008).

2. Systemic Medicine
According to Verma and Heffernan (2008), systemic treatments that can be given
to tinea corporis are:
a. Griseofulvin
Griseofulvin is the first choice systemic drug. The dosage for children is 15-20
mg / kg / day, whereas for adults it is 500-1000 mg / day
b. Ketoconazole
Ketoconazole is used to treat tinea corporis that is resistant to griseofulvin or
topical therapy. The dose is 200 mg / day for 3 weeks.
c. Relatively new drugs such as itraconazole and terbinafine are said to be
satisfactory for the treatment of tinea corporis.

8. What is the first treatment of the scenario ?

a. Non-Pharmacotherapy
1. Maintain body hygiene
2. Use clothes that absorb sweet, are loose and made of cotton
3. Avoid excessive heat or humidity

b. Pharmacotherapy

pg. 30
 1. Ketoconazole 200 gr, 2 x 1
2. 6% benzoic acid, 3% salicylic acid to treat infections and
inflammation are applied to the infected area.
3. Antifungal
Miconazole 2% ccream, suitable for use in intertriginous areas,
smeared thinly to prevent maceration effect, used within 2 weeks.
4. Antibiotics
Erythromycin is the drug of choice. One gram a day (4x250 mg) for 2-
3 weeks.

9.Explain perspective islam!

ْ ‫طفُ ْواٌفَ ِانَـهٌٌُاليَ ْد ُخ ُل‬

ٌ‫ٌٌال َجنَـةٌٌَاِالن َِطيْف‬ َ َ‫اَ ْ ِال ْس ََل ُمٌٌن َِطـيْفٌٌفَتَـن‬
)‫ٌ(رواهٌالبيهقى‬
Artinya:
Islam itu adalah bersih, maka jadilah kalian orang yang bersih. Sesungguhnya
tidak masuk surga kecuali orang-orang yang bersih (H.R. Baihaqi)

pg. 31
 REFERENCE
1. Djuanda, Adhi. 2018. Ilmu Penyakit Kulit dan Kelamin. Edisi
ketujuh.Jakarta : FKUI.
2. Bloom William, Don W. Fawcett. 2002. Buku Ajar Histologi. Edisi 12.
Terjemahan Jan Tambayong. Jakarta: EGC.
3. Khairunnisa Rahadatul ‘Aisy Sodikin. 2018. Candidiasis Kutis
Intertriginosa. Purwokerto : Smf Ilmu Kesehatan Kulit Dan Kelamin Rsud
Prof. Dr. Margono Soekardjo Fakultas Kedokteran Universitas Jenderal
Soedirman Purwokerto. Hal. 15.
4. Price, Sylvia Anderson. 2006. Patofisiologi Konsep Klinis Proses-Proses
Penyakit. Edisi 6 Volume . Jakarta: EGC. Hal 1450-1452
5. Soedarto. 2007. Sinopsis Kedokteran Tropis. Cet.1 Suarabaya: Universitas
Airlangga. Halaman 281,294,332-33
6. Wirya Duarsa. Dkk. 2010. Pedoman Diagnosi dan Terapi Penyakit Kulit
dan Kelamin. Denpasar : Fakultas Kedokteran Universitas Udayana.
7. Budimulja, U. sunoto. Dan Tjokronegoro. Arjatmo. 2008. Penyakit Jamur.
Jakarta : Fakultas Kedokteran Universitas Indonesia.
8. Samuel Rian Wowor; Herry E. J. Pandaleke; Marlyn Grace Kapantow.
2012. Profil Kandidosis Intertriginosa Di Poliklinik Kulit Dan Kelamin.
Manado.
9. Handoko, Ronny P. 2018. Ilmu Penyakit Kulit dan Kelamin. Hal. 135-136.
Badan Penerbit FK UI.
10. Rifqi Afdila. 2013. Hidrocortison. Medan : Universitas Sumatra Utara. Hal.
13-14
11. Hendri Saputra. 2010. Tinea Incognit. Hal. 6
12. Jienshi Pantow; Everly Corputty; Thadea Tandi. 2014. Laporan Kausus
Kulit & Kelamin Kandidiasis Intertriginosa. Manado : Ilmu Kulit Dan
Kelamin Fakultas Kedokteran Universitas Sam Ratulangi. Hal. 1-5.
13. Linuwih, Sri. Bramono, K. Indriatmi, W. 2018. Buku Ilmu Penyakit Kulit
dan Kelamin Edisi 7. Jakarta: Badan Penerbit FKUI. Hal. 19 & 45.

pg. 32
14. Elvina, PA. 2011. Hubungan Rasa Gatal dan Nyeri Vol. 38 No. 4. SMF
Ilmu Kesehatan Kulit dan Kelamin RSUD Wangaya, Denpasar, Bali,
Indonesia. Hal. 265.
15. Herwanto, N. Hutomo, M. 2016. Jurnal Studi Retrospektif:
Penatalaksanaan Dermatitis Atopik Vol. 28 No. 1. Departemen/Staf Medik
Fungsional Ilmu Kesehatan Kulit & Kelamin Fakultas Kedokteran
Universitas Airlangga/RSUD Dr. Soetomo Surabaya. Hal. 50.
16. Faisal Jamin. Akibat Infeksi Candida Albicans Dan Pemberian Kortikosteroid
Menyebabkan Kondisi Imunosupresi Organ Bursa Fabricius Pada Ayam
Pedaging. Banda Aceh : Repository Fakultas Kedokteran Hewan Universitas
Syiah Kuala. Hal. 69.
17. M. Handika. 2016. Kortikosteroid. Padang : Repository FK UNAND. Hal. 3.
18. Handoko Rp. Viral Diease. Skin and Sex Disease. 4th edition. Jakarta: Faculty
of Medicine, University of Indonesia, 2005; 110-2.
19. Samuel Rian Wowor; Herry E. J. Pandaleke; Marlyn Grace Kapantow. 2012.
Profil Kandidiosis Intertriginosa Di Poloklinik Kulit Dan Kelamin. Manado
20. Faderman, D. G., Reid, M. C., Feldman, S. R,. Greenhoe, J., & Krisner, R. S.
2001. The primary care provider and the care of skin disease: the patient’s
perspective. Archives of dermatology, 137(1),25-29.

pg. 33