1P.

01
SEPTEMBER 04,2021

INTRODUCTION TO DERMATOLOGY
DR. KAREL HELDEN M. CLORES-DATOR

TOPIC OUTLINE Cells of the Epidermis

I. THE SKIN III. DERMATOLOGIC Cells Function
A. Layers of the skin EXAMINATION
Keratinocytes Produces keratin, a
1. Epidermis A. Cutaneous signs
2. Dermis 1. Primary lesions
complex filamentous
3. Hypodermis 2. Secondary protein that forms the
B. Skin appendages lesions surface coat of the
1. Sweat glands B. Diagnostic details epidermis, hair, and nails
2. Sebaceous of lesions Melanocytes Dendritic cell that
glands C. Documenting a produces melanin, (skin
3. Hair dermatologic exam pigmentation)
4. Nail IV. MEDICATIONS IN
5. Muscle DERMATOLOGY
Langerhans cells Recognition, uptake,
II. HISTORY TAKING V. REFERENCES processing and
A. General data presentation of antigens to
B. Chief complaint sensitized T lymphocytes,
and History of [Antigen presenting cells
present illness of the skin]
C. PMH Merkel Cells Act as slow adapting
D. Medication history
touch receptors
E. Allergies
F. Social History (mechanoreceptors)
G. Family history
Layers of Epidermis
I. THE SKIN
 Heaviest single organ of the body > 15% of total
body weight
 Functions:
o Protection
o Regulation of body temp [producing sweat
when hot]
o Metabolic Function
o Sense organ
 Meissner corpuscle-light touch
 Paccinian corpuscle-pressure
 Free nerve endings-pain [palm and sole Stratum Corneum/ Horny Layer
mostly kya masakit pag nasugat]  Outermost
 Ruffini’s cells-heat  Structureless, hydrated keratinized dead cells
 Krause cells-cold flattened into horny plates which are continuously
sloughed off or desquamated [skin ngpapalit every 13
A. LAYERS OF THE SKIN days]
A1. EPIDERMIS  [In dermatitis or any skin condition where there is
scaling that is the composed of stratum corneum]
 Derived from ectoderm
Stratum Lucidum
 Stratified squamous keratinizing epithelium
 [Not always present in the cross section of skin, only
 Cells:Keratinocytes(90%),Melanocytes,
found on the thick skin of palms and soles]
Langerhans cells, Merkel cells
 Few layers of flattened closely compacted cells
 Thickest: Palms and soles
 Absent nuclei, increased amount of intercellular
substance, refractile droplets in the cytoplasm make it
look translucent
 Seen only in thick skin (palms and soles)
 [Mas homogenous color compare sa S. corneum]
Stratum granulosum
 3 layers of flattened, rhombic cells with their long axis
parallel with the surface of the skin
 Contain basophilic keratohyaline granules which are
rich in proline and sulfur containing amino acids [resp.
for CHON synthesis in the skin]

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Stratum spinosum or prickle cell layer B.SKIN APPENDAGES
 Polyhedral shaped keratinocytes with delicate
processes or spines projecting from their surfaces
 Spines serve as intracellular bridges for attachment
and nutrient diffusion
 [Seen in dermapathology in cases like dermatitis (cells
are separated from each other)]
Stratum basale
 Lowermost single layer
 Made up of columnar cells resting perpendicular to a
well- defined basement membrane
 Highest mitotic activity  Sebaceous gland produces sebum
 1 melanocyte: 10 basal keratinocytes  Apocrine gland produces sweat, both are attached to
 Difference in skin color of different races is due to hair follicle.
quantity and quality if melanosomes and not due to  Eccrine gland empties directly into the skin surface.
number of melanocytes
 Pale skin: fewer, smaller, packaged B1. SWEAT GLAND
 Dark skin: more melanosomes, larger, singly dispersed a. Eccrine gland
 Small sweat glands found predominantly on
A2. DERMIS palms, soles and forehead
 Derived from the mesoderm  Functions for thermoregulatory control
 Composed of dense, irregularly arranged connective  Stimulus is heat
tissue b. Apocrine gland
 Principal component: collagen (type I)  Large sweat glands located in axilla, mammary
 Provides mechanical support and vascular bed for glands, areola, genital area
metabolic exchange processes  Apocrine sweat: odorless until it reaches the skin
 Thickest at the base surface where it is altered by bacteria (when
acted upon by bacteria, responsible for the body
odor)
B2. SEBACEOUS GLANDS
 Produces lipids that contribute to barrier function
 Found all over the body except palms and soles
 Largest concentration on the face and scalp –
“seborrheic areas” [even the chest and upper back]
 Divided into 2 layers
o Papillary layer or sub epithelial layer
 Superficial layer consists of loose connective
tissue with collagenous and elastic fibers, and
nervous papillae
o Reticular layer
 Deeper, relatively thick layer consists of
coarse collagenous fibers [mas makakapal
ang collagen fiber]
A3. SUBCUTANEOUS TISSUE/HYPODERMIS/PANNICULUS
 Consist mainly of adipose tissue B3. HAIR
 Provides mobility  Protection, regulation of body temperature
 Thickest: abdomen and buttocks  Stages of development
 Thinnest: eyelids and scrotum [kaya manipis ang o Anagen – active growth phase; 85-90% of scalp
eyelids natin] hair
o Catagen – involution phase [stop in growth]
o Telogen – total arrest in growth

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 B4. NAIL
 act to assist in grasping small objects and in
protecting the fingertip from trauma
 Fingernails growth: 0.1 mm/day (4–6 months to
replace a complete nail plate)
 Toenail growth: slower,12–18 months required to
replace the great toenail
B5. MUSCLES
 arrectores pilorum (erectors of the hairs) =
gooseflesh
 tunica dartos (or dartos) of the scrotum
 in the areolas around the nipples
II. HISTORY TAKING
A. GENERAL DATA
 Age
 Gender
 Occupation [eg. Nurses always use gloves – consider
contact dermatitis secondary to gloves]
B. CHIEF COMPLAINT AND HISTORY OF PRESENT ILLNESS
 Duration [acute or chronic]
 Periodicity [time of the day it gets worse]
 Evolution [first lesion that appeared, usually a vesicle or
bulla]
 Location [arthropod bite – extremities]
 Symptoms (pruritus, pain, bleeding – malignancies
(SCC)
 Severity [not so pruritic: psoriasis; very pruritic: atopic
dermatitis]
 Ameliorating and Exacerbating Factors [oil, pressure
eg. Tinea infections mas lalong kumakati pag
nakukulob]
 Preceding illness, new medications, new topical
products, or exposures
 Therapies tried, including over-the counter or home
remedies, and response to therapy [e.g use of
hydroquinone]
 Prior similar problems, prior diagnosis, results of biopsies
or other studies performed [e.g psoriasis, scleroderma]
C. PAST MEDICAL HISTORY
 chronic illnesses (diabetes, renal and hepatic disease,
infection with HIV or hepatitis viruses, polycystic ovarian
syndrome, lupus, thyroid disease)
 those that are associated with skin disease (asthma,
allergies)
 History of surgical procedures
 Immunosuppression (esp. HIV or genital lesions)
 Pregnancies (restrict medications)
 Psychiatric disease (just evaluate by yourself)
 History of blistering sunburns, exposure to arsenic or
ionizing radiation (if suspecting CA) [how to quantify
allergies? Wheal/ “pantal”]
D. MEDICATION HISTORY
 Prescription
 Over-the-counter medications
 Vitamins and dietary supplements (may sometimes
cause hypersensitivity reactions)
 Herbal remedies (if overdone, may aggravate erosion
of lesion)
E. ALLERGIES
 Medications
 Food
 Environmental antigens
 Contactants - can be elicited if patient have had
patch test before
F. SOICIAL HISTORY
 hobbies and leisure activities
 alcohol and tobacco use
 illicit drug use
 sexual history
 dietary history
 bathing habits [longer bathing time skin becomes
drier]
 pets [consider pediculosis]
 living conditions [e.g scabies]
 history of travel [e.g deep wounds- consider
cryptococcosis or histoplasmosis]
G. FAMILY HISTORY
 skin disease
 atopy (atopic dermatitis, asthma, allergic rhinitis) –
Atopic triad
 skin cancer
III. DERMATOLOGIC EXAMINATION
A. CUTANEOUS SIGNS
 Primary lesion - original lesion
 Secondary lesion - result of modification of primary
lesions by regression, trauma or other factors
A.1. PRIMARY LESIONS
1. MACULE
 Flat, non-palpable lesions <1 cm in diameter
 Macules represent a change in color and are not
raised or depressed compared to the skin surface
 e.g Lentigo
 Decription: solitary, hyperpigmented macule

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2. PATCH 7. WHEAL [“Pantal” in Tagalog]
• Flat, non-palpable lesions >1 cm in diameter.  Evanescent, edematous, plateau-like elevation of
• e.g Impetigo various sizes
 Oval or arcuate contours, pink to red surrounded
by a flare of macular erythema that may be
discrete or coalesce [Appears when bitten by an
insect and you scratched it]

3. PAPULE
 Elevated lesions <1 cm in diameter that can be felt
or palpated
 e.g Molluscum contagiosum
8. VESICLE
• Circumscribed, small, clear, fluid-filled blister <1 cm
in diameter
• e.g. Herpes simplex or varicella

4. PLAQUE
 Palpable lesions >1 cm in diameter that are
elevated or depressed compared to the skin surface
[Equivalent of patch but it is elevated]
9. BULLAE [Bigger version of vesicle]
• Circumscribed, small, clear, fluid-filled blister >1 cm
in diameter [Sometimes it can be hemorrhagic]
• When you touch it, it can be tense, fluctuant or
flaccid

 Psoriasis - Erythematous plaque with white scales

5. NODULE
 Firm papule or lesion that extend into the dermis or
subcutaneous tissue [If you touch the lesion, it is
deep into the dermis]
 e.g Furuncle 10. PUSTULE [Very common]
 Small elevations of the skin that contain purulent
material
 e.g Folliculitis

6. TUMOR
 Firm and freely movable or fixed masses of various
size and shape, generally are 2 cm in diameter
[Merkel cell carcinoma: rare carcinoma of the
skin] A.2. SECONDARY LESIONS
1. SCALES
 Dry or greasy laminated masses of keratin
 Fine, delicate, branny, coarse [Stratum corneum
that became thick is the one that is sloughing off]

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  Right upper Picture: White laminar scaling of
psoriasis (laminar means they peel in layers)
 Lower picture: Tinea corporis – firm and delicate
 Right lower Picture: Sebborheic dermatitis (yellowish
and greasy)]
2. CRUSTS
• Dried serum, pus or blood usually mixed with
epithelial or bacterial debris
Previously a bullae but it ruptured and the top of the
• Dry, golden yellow, soft, friable
bullae was removed
6. ULCERS
 Rounded or irregularly shaped excavations that
result from complete loss of the epidermis plus
portions of the dermis & subcutis

Left picture: Impetigo contigiosa caused by S. aureus

that produces golden yellow crustings (initially there
can be papules and vesicles, that’s why it is important
to ask the patient the initial appearance of the lesion)
Right picture: Discoid lupus erythematosus Cause scarring because it reach the subcutaneous
(erythematous to hyperpigmented plaque with 7. SCAR
hemorrhagic crust) • Composed of new connective tissue that replaced
3. EXCORIATIONS AND ABRASIONS lost substance in the dermis or deeper parts as a
 Punctate or linear abrasion produced by result of injury or disease, as part of the reparative
mechanical means [like sratching], usually process
involving the epidermis but not uncommonly
reaching the papillary layer of the dermis

 Can be depressed (scars in acne vulgaris) or

Patients with atopic dermatitis can also present with
excoriations as a secondary lesion, also those with
lichen simplex chronicus or those with chronic dermatitis
can present with excoriations as a sign that the patient
scratched the lesion.
4. FISSURES
 Linear cleft through the epidermis or into the dermis
 May be single or multiple and vary from
microscopic clefts several centimeters in lengths
with sharply demarcated margins
 Heel fissures or cracked heel
 Usually happens because of a very dry skin
accompanied by pressure on the area
 Common especially in the elderly
5. EROSIONS
 Loss of all portions of the epidermis
 May or may not become crusted, but it heals
without a scar [contrary to ulcer which heals with
scarring because it reaches the dermis]
elevated (hypertrophic scar and keloid)
 Right picture: keloid from vaccination scar
 Keloid can become very large and if it is on the
chest due to acne, it can merge and form larger
masses.
B. DIAGNOSTIC DETAILS OF LESIONS
 Number – single, multiple, few (2-3 lesions)
 Distribution – generalized/localize, discrete/confluent,
group
 Color – erythematous, hyper/hypopigmented
 Configuration – annular, linear, serpiginous, targetoid
 Primary lesion – macule, patch, papule, etc.
 Secondary lesion- scale, crust, ulcer, etc.
 Location – flexurals, extensors, sun-exposed, etc.
 Diagnostic details of lesion are used to described
lesion.
 These terminologies will be put together to be able
to form a complete dermatological physical
examination

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1. Number
 Solitary/multiple

1st picture: Solitary hyperpigmented papule

2nd picture: Multiple hyperpigmented papules Case of epidermal nevus following lines of blaschko
2. Distribution Epidermal nevus follows dermatomal and lines of
 Generalized/localized blaschko
3. Evolution [Usually, it was not reported in the derma
physical exam]
 Development from primary lesion to a secondary
lesion

 Generalized – no need to put location of lesion

 Localized – need to put location of lesion
 Symmetrical/asymmetrical

 1st picture: primary lesion – bullae and vesicle

 2nd picture – bullae ruptured – formed crusts and
erosion (roof of bullae was removed exposing skin)
4. Involution [What happened to skin condition when it
heals]
 Resolution - No marks at all, skin back to normal
 Psoriasis with Symmetrical lesion after it heals
 Symmetrical if you put a line in the midline, right  Hyperpigmentation - Darkening of skin after skin
side is like left side. condition; Acne marks from acne vulgaris
 Dermatomal

 Hypopigmentation
o Skin with lesion is lighter than the normal skin
Can Happen when treated with topical
steroid
o Hypo/hyperpigmentation not permanent, go
back to normal within 6 months.
Dermatomal seen in herpes zoster, sometimes in
incontinentia pigmenti (rare congenital condition),
epidermal nevus.
 Following lines of cleavage [Lines produce when
stand against gravity, and the skin sags]
 Scar

 Hypertrophic or keloidal
Pityriais rosea follows line of cleavage, triangular  acne on the chest in keloid former
Christmas tree pattern individual.
 Individual acne marks merge forming a
 Lines of Blaschko [Embryonic in origin, not visible; large keloid.
Left by epidermal migration of the cells of the skin]

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5. Configuration  Guttate
 Linear

 Resembles line
 Resembles water drops
 Striae distensae / stretch marks
 Guttate psoriasis
 Description: erythematous to hyperpigmented
linear plaques  Nummular
 Annular

 Circular lesion with central flaring

 Resembles ring  Also known as Discoid or Coin shape
 Tinea corporis  Circular lesion
 Description: solitary annular erythematous  Nummular dermatitis
plaque with scaling  Description: solitary nummular erythematous plaques
with crust and scales
 Arcuate
6. Color
 Erythematous [Red]

 Like annular but not complete circle

 Erythema gyratum repens- a rare condition,
inflammatory skin condition associated to  lesion of psoriasis
malignancy  Violaceous
 Description: multiple arcuate erythematous
plaques
 Polycyclic

 Picture above: Senile purpura seen in elderly

 Skin of elderly are fragile when you put friction
can cause bruising
 multiple annular lesions that are closed together  Other conditions: lichen planus – present like
wheals of urticarial psoriasis with scales but violaceous
 Description: multiple polycyclic erythematous  Yellow
wheals
 Serpiginous

 Xanthelasma - Yellowish plaques over eyelids

(upper and lower)
 Resembles snake  Can also occur in other parts of the body, not
 Cutaneous larva migrans (migration of hookworm usually appreciated
larva in the skin that leaves tract)

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  Salmon colored extravascular, or the RBCs are already
extravasated)

 Lighter version of erythematous

 Pityriasis rosasea
 Hyperpigmented
8. TESTING FOR ANESTHESIA/HYPOSTHESIA

 Dark
 Pigmented Nevus
 Hypopigmented Lesions [lesion that is lighter than
 Tool used to assess sensation of the skin. The pins are
the color of the skin]
of different sharpness (pointed/dull) and thickness.
 This is usually done if the patient is suspected of
having Leprosy or Hansen’s Disease
 In lieu of this specific tool, tip of ballpen or pencil
can be used instead and assess the patient by
asking whether they can feel the sensation as blunt
(eraser part) or sharp (tip of the pencil/pen)
 If the patient reported negative sensation, or even
diminished sensation (hyposthetic) it is a
 Document as: Multiple, hypopigmented macules
characteristic of an anesthetic lesion (Hansen’s
and patches at the back
Disease or Leprosy)
 Diagnosis: Pityriasis versicolor (an-an
 Depigmented Lesions (devoid of pigment/no C. DOCUMENTING A DERMATOLOGIC EXAMINATION
melanin)
[combination of classifying the lesion]
1. Number (solitary or multiple)
2. Distribution (Generalized or Localized)
3. Configuration
4. Color
5. Primary lesion
6. Secondary lesion
7. Location (usually, when the lesion is generalized,
Document as: Multiple, depigmented patches on the localization can be omitted)
face SAMPLE DERMATOLOGIC DIAGNOSIS
Diagnosis: Vitiligo Diagnosis: Psoriasis
7. Consistency [Touching the lesion is not usually advised, Document as:
especially if the lesion is suspected to be infectious] Multiple, generalized, guttate,
 Soft erythematous papules and
 Firm or indurated plaques with whitish scaling

Often disregarded unless you are considering lesions Tinea corporis

like furuncles/nodules to assess whether these lesions Multiple, localized,
are fluctuant or not polycyclic/annular
erythematous plaques with
 Dermoscopy [Done by using a glass slide and
scales on the left axilla
pressing it on top of the lesion]
o Blanching - if the lesion is erythematous but
not a vasculitis, the lesion will blanch
(meaning the erythema is intravascular)
o Non blanching - if the lesion is pressed but
retains its erythematous or violaceous color,
then it is vasculitis (the color of the lesion is

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 Vitiligo
Multiple, generalized, (no  A particular potency is used for a certain part of
pattern=no configuration), the body
depigmented, patches (no  Superpotent corticosteroids (Class I Steroids)
secondary lesion) o Clobetasol propionate
(generalized, therefore no o Halobetasol propionate
need to mention location) o Betamethasone diproprionate
 Mid Potent Corticosteroid
o Betamethasone valerate
Psoriasis o Mometasone furoate (Elica)
Multiple, localized, (no o Fluocinolone acetonide
configuration), erythematous o Fluticasone propionate
papules and plaques with  Least potent Corticosteroid
whitish scaling over the left o Hydrocortisone
hand  Superpotent ones are used in atopic dermatitis
that are resistant (usually, atopic dermatitis
responds to mid potent corticosteroid)
 Discoid lupus erythematosus and other dermatitis
IV. MEDICATIONS USED IN DERMATOLOGY – Class 1 corticosteroids
A. TOPICAL CORTICOSTEROIDS  Least to mild potent are used in areas that are thin
 [most commonly prescribed medication in skin (e.g. face, neck, axilla and inguinal area)
dermatology, almost all dermatologic conditions  If the lesion is thick and it involves the thick skin like
respond to topical medications] palms and soles, extremities or trunk, superpotent
 Reduces the symptoms of inflammation but may not corticosteroids may be used)
address the underlying cause of the disease  DO NOT GIVE CLOBETASOL FOR LESIONS LOCATED
 MOA: ON THE FACE FOR A LONG TERM (may be
o mediated by binding of the corticosteroid to its considered if the lesion is discoid lupus
receptor in the cytosol - translocation to the erythematosus)
nucleus at the corticosteroid response element -
inhibit transcription of inflammatory proteins B. SYSTEMIC ANTIHISTAMINES
 Topical steroids are divided into groups based on their
 MOA:
strengths:
o Inverse agonists that reversibly bind and stabilize
o strongest steroids are in group I
the inactive form of H1 receptor
o weakest steroids are in group VII
o Anti-pruritic effects
o important to know the potency of the medication
 Classes
because it has different uses. A particular potency
1. First generation – not protein bound therefore can
is used in a certain part of the body
cross the BBB=Sedating)
 Risks and precautions
 Chlorphenamine
o Highly potent steroids should be used for short
 Diphenhydramine
periods of time intermittently (2-3 weeks)
 Hydroxyzine
o Do not stop immediately, taper it
2. Second generation – protein bound = cannot
o It should be avoided on ulcerated or atrophic or
cross BBB= non-sedating)
infected skin (may aggravate infection and
 Cetirizine
atrophy)
 Desloratidine
o Sudden discontinuation after prolonged use
 Ebastine
should be avoided to prevent rebound
 Levocetirizine
phenomena
 Loratidine
o Superpotent topical steroids should be used with
 Must know if you are giving a sedating or non-
caution in children and elderly as well as in thin
sedating antihistamine
areas of the skin such as the face and genital
C. ANTIBIOTICS
region
 Complications 1. TOPICAL
o Acne (common)  Used in impetigo, acne vulgaris, rosacea
o Atrophic changes, telangiectasia, purpura, easy  Examples
bruising, striae formation (common in psoriasis px o Mupirocin ointment –[impetigo]
with continuously using steroid), ulceration  MOA: inhibition of tRNA;
o Acneiform eruptions [common in COVID patients  Used for G (+) infections such as
due to giving of systemic steroids] Staphylococcus sp.
o Hypertrichosis o Oxytetracycline ointment -[impetigo]
o Hypopigmentation  MOA: inhibition of 30s ribosome;
o Development of infections  For G (+/-) organisms
o Allergic reactions (most common: Budesonide) o Clindamycin gel - [acne vulgaris, rosacea]
o Systemic effects such as glaucoma and  MOA: inhibition of 50s ribosome;
suppression of HPA axis.
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  For G (+) organisms such as
Propionibacterium acnes
2. SYSTEMIC
 Skin infections are usually caused by
Staphylococcus and Streptococcus sp.
 Examples:
o Cefalexin
 Adults
- 250 and 500 mg tablets
- Q6
 Pediatric
- 125mg/5mL or 250mg/5mL
- 20-50 mg/kg/ day
- Q6
o Cloxacillin
 Adults
- 250 and 500 mg tablets
- Q6
 Pediatric
- 125mg/5mL
- 50-100 mg/kg/day
- Q6
o Co-amoxiclav
 Adults
- 375 and 625 mg tablets
- Q8 to Q12
 Pediatric
- 156.25mg/5mL
- 40 mg/kg/day
- Q8

REFERENCES
1. Dator, K., Introduction to Dermatology. [powerpoint slides]
2. Sidenotes

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