0% found this document useful (0 votes)

76 views168 pages

Lichen Simplex Chronicus Overview

Uploaded by

krishnan

We take content rights seriously. If you suspect this is your content, claim it here.

Available Formats

Download as PDF, TXT or read online on Scribd

0% found this document useful (0 votes)

76 views168 pages

Lichen Simplex Chronicus Overview

Uploaded by

krishnan

We take content rights seriously. If you suspect this is your content, claim it here.

Available Formats

Download as PDF, TXT or read online on Scribd

What’s included: Ready-to-study anatomy, physiology and pathology notes of the integumentary system presented
in succinct, intuitive and richly illustrated downloadable PDF documents. Once downloaded, you may choose to
either print and bind them, or make annotations digitally on your iPad or tablet PC.
(BLUE = CLICKABLE HYPERLINK)
- OVERVIEW OF SKIN STRUCTURE & FUNCTION
- GENERAL PRINCIPALS OF DERMATOLOGY
- BENIGN CYSTIC SKIN LESIONS
o EPIDERMAL CYST
o PILAR CYST (TRICHILEMMAL CYST)
o GANGLION CYST
o MILIUM
- BENIGN FIBROUS SKIN LESIONS
o DERMATOFIBROMA
o SKIN TAGS
- BENIGN HYPERKERATOTIC LESIONS
o SEBORRHEIC KERATOSIS
o CORNS / ‘HELOMATA’
- BENIGN PIGMENTED LESIONS
o CONGENITAL NEVOMELANOCYTIC NEVI (‘BIRTH MARK’)
o ACQUIRED NEVOMELANOCYTIC NEVI (COMMON MOLE)
o ATYPICAL NEVUS (DYSPLASTIC NEVUS)
o EPHELIDES (FRECKLES)
o SOLAR LENTIGO
- VASCULAR LESIONS
o HAEMANGIOMAS
o PORT-WINE STAINS
- ACNEIFORM ERUPTIONS
o ACNE VULGARIS (COMMON ACNE)
o ROSACEA
- DERMATITIS (ECZEMA)
o ACUTE DERMATITIS/ECZEMA
o SEBORRHEIC DERMATITIS
o STASIS DERMATITIS (VENOUS ECZEMA)
o LICHEN SIMPLEX CHRONICUS
o ERYTHEMA MULTIFORME
- PAPULOSQUAMOUS DISEASES
o LICHEN PLANUS:
o PITYRIASIS ROSEA
o PSORIASIS
- VESICULOBULLOUS DISEASES
o BULLOUS PEMPHIGOID
o PEMPHIGUS VULGARIS
o DERMATITIS HERPETIFORMIS
o PORPHYRIA CUTANEA TARDA
- DRUG ERUPTIONS
o MORBILLIFORM DRUG REACTIONS
o URTICARIAL DRUG REACTIONS
- HERITABLE DERMATOSIS
o ICHTHYOSIS VULGARIS
o NEUROFIBROMATOSIS 1
o VITILIGO
- BACTERIAL INFECTIONS
o IMPETIGO (SCHOOL SORES)
o ERYSIPELAS
o CELLULITIS
o FOLLICULITIS
o FURUNCLES (BOILS) & CARBUNCLES
- FUNGAL INFECTIONS
o PITYRIASIS (TINEA) VERSICOLOR
- PARASITIC INFECTIONS
- PARASITIC INFECTIONS
o SCABIES
o LICE (PEDICULOSIS)
- VIRAL INFECTIONS
o HERPES SIMPLEX
o CHICKEN POX (VARICELLA ZOSTER)
o HERPES ZOSTER (SHINGLES)
o MOLLUSCUM CONTAGIOSUM
o HPV WARTS (VERRUCA VULGARIS)
- PREMALIGNANT & MALIGNANT SKIN CONDITIONS
o ACTINIC KERATOSIS (SOLAR KERATOSIS)
o BASAL CELL CARCINOMA
o SQUAMOUS CELL CARCINOMA
o KERATOACANTHOMA
o MALIGNANT MELANOMA
- PEDIATRIC EXANTHEMS
o MEASLES VIRUS
o RUBELLA VIRUS (“GERMAN MEASLES)
o HUMAN PARVOVIRUS B19 (“5TH DISEASE”)
o SCARLET FEVER
o SCALDED SKIN SYNDROME (SSS)
o TOXIC SHOCK SYNDROME (TSS)
- PROCEDURAL DERMATOLOGY
- SKIN PATHOLOGY – UNDER A MICROSCOPE
- EXAMPLES OF EXAM QUESTIONS
OVERVIEW OF SKIN STRUCTURE & FUNCTION
OVERVIEW OF SKIN STRUCTURE & FUNCTION

Functions of Normal Skin:

• Mechanical barrier
• Chemical barrier
• Prevent Fluid Loss (Overlapping Cells & Intercellular Lipid → Minimises loss of Water)
• Defence against micro-organisms
• Immunological barrier
• Endocrine organ – (Produces Vitamin-D under UV)
• Vitamin D → Maintains Calcium Homeostasis (↑Ca+ Absorption in Gut & ↑Renal Ca+ Retention)
• Melanin → Protects against UV
• Thermoregulation – (Varying blood flow →Allows heat Conservation or Evaporative Cooling)
• Sensory organ

Basic Structure of Normal Skin:

- 3 Layers:
o Epidermis (Top Cellular Layer):
§ Keratinocytes
§ Melanocytes
§ The 5 Layers of the Epidermis:
• 1) Stratum Germinativum/Basale:
o Single layer of cuboidal/columnar cells
• 2) Stratum Spinosum (Prickle Cell layer):
o Several layers of polyhedral cells
• 3) Stratum Granulosum:
o 3-5 layers flattened cells
• 4) Stratum Lucidum:
o (Present only on very thick layers of epidermis (Eg: Glabrous Skin
[palms/feet]))
o = The Lucid layer of Flattened Cells before Stratum Corneum
• 5) Stratum Corneum:
o 5-50 layers of Flattened, Dead Cells (Squames)
o Protective Barrier; Holds in Moisture
o Cytoplasm is filled with keratin & keratohyalin granules
o Dermis (Middle Fibrous Layer):
§ Connective Tissue
§ Blood Vessels
§ Nerves (Sensory Receptors & Free Nerve Endings)
§ Hair Follicles + Arrector Pili (the Smooth Muscle)
• Note: Skin without hair – (Eg: Palms & Soles) = “Glabrous Skin”
• Note: Skin With Hair – (Ie: Rest of the body) = “Non-Glabrous Skin”
§ Glands (Sweat, Sebaceous)
§ Contains Some Cells:
• Fibroblasts: Synthesis and degradation of connective tissue
• Histiocytes/Macrophages: Phagocytic cells
• Mast cells: Secretory cells →Vasoactive Mediators (histamine) → Skin Allergies
• Lymphocytes: Small number collect around blood vessels in normal skin
§ 2 Layers:
• (R) - Reticular Layer (thick Collagen, lower layer) - much stronger
• (P) - Papillary layer (fine Collagen, upper layer) – weaker
o Hypodermis (Fat Layer):
§ Adipose Tissue
§ Functions:
• Insulates the body
• Stores Energy
CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons
LAYER 1: THE EPIDERMIS:
- Structure of the Epidermis:
o Most Superficial Layer of Stratified Squamous Keratinised Epithelium
o Avascular
o Almost Entirely Cellular:
§ 95% of Epidermal Cells are Keratinocytes (Produce Keratin)
§ Other Cells include: Melanocytes, Merkel Cells & Langerhans Cells
§ Continually regenerating (Rate is just sufficient to replace cells lost from the surface)
o Protective barrier
o Approximately 0.1 to 1mm thick

- The 5 Layers of the Epidermis:

o 1) Stratum Germinativum/Basale:
§ Single layer of cuboidal/columnar cells
§ Basal Cells take 14 days to differentiate → Keratinocytes
§ Keratinocytes take 14 days to be shed off
§ Strongly adherent to the Basement Membrane by Hemidesmosomes

o 2) Stratum Spinosum (Prickle Cell layer):

§ Several layers of polyhedral cells
§ Keratin-Tonofibrils Insert into interconnecting desmosomes from adjacent cells
§ Keratinocytes Contain ‘Lamellar (lipid containing) bodies’:
• Are Secreted into the Extracellular spaces (Sticks Cells Together)
o → Forms a water-barrier
o →Also acts to cement keratinized squames together in Stratum Corneum
§ Langerhans Cells:
• Like Macrophages
• Have Antigen Presenting Capacity
o 3) Stratum Granulosum:
§ 3-5 layers flattened cells
§ Loss of nuclei
§ Keratinocytes:
• Keratohyalin granules (Composed of Profilaggrin, Keratin Filaments, & Loricrin)
o Keratohyalin = Protein involved in Keratinisation
o Note: Eczema is probably due to a mutation in Profilaggrin
• Lamellar Body secretions:
o Lamellar Body Contents Discharged into Intracellular Spaces
§ (Lipids, Enzymes)
o – Acts like the “Mortar” between the cellular “Bricks”

o 4) Stratum Lucidum:
§ (Present only on very thick layers of epidermis (Eg: Glabrous Skin [palms/feet]))
§ = The Lucid layer of Flattened Cells before Stratum Corneum
• Cells have No nuclei or organelles
o 5) Stratum Corneum:
§ 5-50 layers of Flattened, Dead Cells (Squames)
• Devoid of Nuclei & Organelles
§ Protective Barrier; Holds in Moisture
§ Cytoplasm is filled with keratin & keratohyalin granules
§ Cells are stuck together by contents of Lamellar Bodies
§ Thicker on Glabrous Skin (Palms and soles)

C = Corneum; L = Lucideum; G = Granulosum; S = Spinosum; B = Basale

- Cellular Component of the Epidermis:
o Keratinocytes – (In all Layers):
§ Form the Keratinized Stratified Squamous Epithelium
§ Contain Keratin (Protein) Intermediate Filaments in the Cytoplasm
§ Keratin:
• Two types of epithelial keratins:
o Type I (acidic)
o Type II (basic)
o (Note: Each are produced in Equal Amounts)
• Keratin Proteins Polymerise as Heterodimers:
o Type 1 + type 2 → Polymers
• Keratin Polymers aggregate → Keratin Filaments
• Keratin Filaments aggregate → Tonofilaments
§ “Keratinisation” – Keratinocytes Differentiate as they Migrate Upwards:
• Formation of Keratin proteins in Cytoplasm
• →Aggregation of the Keratin Filaments into ‘Tonofilaments’ (Like a rope)
o (Tonofilaments →Anchor Desmosomes to the Cytoskeleton)
§ Join to Adjacent Cells via:
• Desmosomes:
o Intercellular attachments between keratinocytes
• Hemidesmosomes:
o Attachment of the Basal Keratinocytes (Epidermis) to the Basement
Membrane (Dermis)
o Very Tight Connection

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

o Melanocytes – (In Stratum Basale):
§ Pigment Cells – Synthesise Melanin Pigment
• Melanin contained in Melanosomes
• Transferred to keratinocytes via Dendritic Processes
• Melanin Absorbs UV radiation
§ Located in Stratum Basale, Dermis and Hair Follicles
§ Note: Differences in Racial Pigmentation:
• Due to ↑Melanocyte Activity (NOT Melanocyte Number)

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

o Merkel Cells – (In Stratum Basale):
§ Nerve Ending Associated
§ Contain small, dense Granules of Catecholamines
§ Located in Stratum Basale
§ - Probably Neuro-Endocrine Function
• Sensory mechanoreceptors
• Closely associated with Nerve Terminal Filaments (free nerve endings)

Source: [Link]

o Langerhans Cells – (In Stratum Spinosum):

§ Antigen Presenting Cells of the Immune System
§ Have long Dendritic Processes that radiate through the Epidermis
§ Located in the Stratum Spinosum
§ Migrate through Epidermis and Dermis to Lymph Nodes
§ - Immune Function

Public domain; Available from: [Link]

- Epidermopoiesis (Epidermal Renewal) & Desquamation (Shedding of Skin):
o (Note: Rate of Epidermopoiesis must = Rate of Desquamation )
§ Stimulated by Growth Factors:
• Epidermal Growth Factor (EGF)
• Transforming Growth Factor a (TGFa)
• Fibroblast Growth Factor (FGF)
§ Inhibited by Cytokines:
• Interferon Gamma (IFNy)
• Tumour Necrosis Factor (TNF)

o Epidermopoiesis (Epidermal Renewal):

§ Epidermis continually renews itself
§ - by Basal (Columnar) Cell Division
§ Turnover rate ≈6 Weeks
§ Basal Cells Become → Keratinocytes (Epidermal Cells):
• Via Keratinization = Synthesis of Keratin Protein
§ Transit time to the stratum corneum is approx 14 days

o Desquamation (Shedding of the Skin):

§ Occurs when desmosomes are degraded (Mediated by Cholesterol Sulphatase)
§ Or by Wear & Tear
§ Desquamation requires another 14 days

Baumann, L. S., & Baumann, L. (2009). Cosmetic dermatology. McGraw-Hill Professional Publishing.
DERMAL-EPIDERMAL JUNCTION:

- Dermal-Epidermal Junction (Stratum Basale: Basement Membrane):

o Where the Stratum Basale of the Epidermis attaches to the Basement Membrane
o Stratum Basale:
§ Basal Cells (Basal Keratinocytes)
• Hemidesmosomes on Basal Cells attach the Epidermis to the Basement Membrane
§ Melanocytes are Interspersed amongst the Basal Cells
• Large Dendritic Cells
• Responsible for Melanin Pigment Production
§ Merkel Cells:
• - Probably Neuro-Endocrine Function
• Contain small, dense Granules of Catecholamines
o Basement Membrane:
§ Lamina Lucida - anchoring transmembrane filaments of the Hemidesmosomes
§ Lamina Densa - (Lattice structure of type IV Collagen)

o Hemidesmosomes:
§ Important in maintaining adhesion between Dermis & Epidermis
§ Associated with Keratin Filaments & Keratin Tonofibrils

o Epidermis & Dermis join in a ripple-like fashion for extra strength (in addition to desmosomes):
§ Rete Ridges (Epidermis)
§ Dermal Papilla (Dermis)

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

LAYER 2: THE DERMIS:

- Structure of the Dermis:

o Mostly Extracellular Matrix:
§ Extracellular Collagen
§ Elastin
o Contains Some Cells:
§ Fibroblasts: Synthesis and degradation of connective tissue
§ Histiocytes/Macrophages: Phagocytic cells
§ Mast cells: Secretory cells →Vasoactive Mediators (histamine) → Skin Allergies
§ Lymphocytes: Small number collect around blood vessels in normal skin
o Also contains Neurovascular & Other Auxiliary Skin Structures:
§ Blood Vessels
§ Nerves
§ Sweat Glands
§ Hair Follicles (And Arrector Pili – The Smooth Muscle of the Hair Follicle)
o 2 Layers:
§ (R) - Reticular Layer (thick Collagen, lower layer) - much stronger
§ (P) - Papillary layer (fine Collagen, upper layer) - weaker

Available from: [Link]

epidermis-is-thrown-into-folds_fig2_281588115
CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons
o Connective Tissue of the Dermis:
§ #1 Collagen = Very tough, fibrous protein – High Tensile Strength
• The Predominant Protein of the Dermis (As opposed to Keratin of the Epidermis)
§ Elastin = Provides Elasticity to Skin – Deformity with Memory

Scientific Figure on ResearchGate. Available from: [Link]

structure-of-healthy-skin-in-which-the-different-layers_fig6_276696375

§ Glycosaminoglycans (GAGs) = Absorb water – Provide Viscosity

• Hyaluronan backbone with glycoprotein branches
LAYER 3: THE HYPODERMIS:

- Structure of The Hypodermis:

o Composition:
§ Mostly Fat (Adipose Cells)-(Thickest in Abdomen)
§ Blood Vessels
§ Nerves
o Functions:
§ Insulates the body
§ Stores Energy

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

AUXILIARY COMPONENTS OF SKIN:
- Vasculature:
o Abundant network of dermal vessels
o Functions:
§ Nutrition of Skin Tissue:
§ Regulation of Body Temperature:
• Conducts heat from Interior to Exterior → Heat loss to Environment
• Vasodilation/constriction Important in Thermoregulation
§ Blood Reservoir:
• Under conditions of circulatory stress (Eg: Exercise/Haemorrhage/Shock),
Sympathetic Stimulation → Vasoconstriction → ↑Circulating Blood Volume

o Cutaneous Circulatory Apparatus – 2 Types of Vessels:

§ 1) Nutritive Vessels:
• Arteries
• Capillaries
• Veins
• (Organized into a horizontal Subdermal Plexus):
o Ascending arterioles extend towards the epidermis
§ Subpapillary Plexus (In the Papillary Dermis)
• Capillaries loop into the dermal papilla
§ 2) Vascular Structures for Heat Regulation:
• Extensive Subcutaneous Venous Plexi:
o Can hold Large quantities of blood
• Arteriovenous Anastomoses:
o Only present in areas of Maximal Cooling (Hands, Feet, Lips, Nose & Ears)
• Note: BOTH Innervated by Sympathetic Adrenergic Vasoconstrictor Fibers:
o Sympathetic NS → Vasoconstriction → Minimal Heat Loss
o (No Stimulation → Vasodilation → Maximal Heat Loss)

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

- Cutaneous Sensory System:
o Sensory Apparatus of the Skin:
§ Most afferent nerve fibres terminate the Face & Extremities (Few on back)
o Sensory receptors:
§ Receptors of touch, pain, temperature, itch and mechanical stimuli
§ Nerve fibers enter the dermis from the underlying adipose tissue
§ 1) Unencapsulated:
• Free Nerve Endings:
o In Superficial Dermis & Epidermis
o Receptors for Pain, Touch, Pressure, & Temperature
o Including Nociceptors:
§ A-Delta Fibres:
• Fast, Sharp, Pricking Pain
• Thick, Myelinated → Fast Conduction
§ C-Fibres:
• Slow, Dull, Aching, Burning Pain
• Thin, Unmyelinated → Slow Conduction
• Merkel Cell Discs (Merkel Touch Spots):
o Found in the Stratum Basale of the Epidermis
o Receptors for Light Touch
• Hair-Follicle Receptors:
o In & Surrounding Hair Follicles
o Mechanoreceptors
§ 2) Encapsulated (Lamellated Capsule):
• Meissner Corpuscles:
o In Dermal Papillae
o Fine Touch receptors
• Pacinian Corpuscle:
o In Deep Dermis & Hypodermis
o Deep Pressure Sensors
• Ruffini Endings:
o In Deep Dermis & Hypodermis
o Directly Associated with Collagen Fibrils → Stretch Receptors

Creative Commons: By Cristina Sala Ripoll; University of Dundee;

[Link]
o Physiology of Sensory Receptors:
§ Concept of Adaption:
• Adaption: Under a maintained stimulus of constant strength, the frequency of action
potentials declines over time
• Slowly-Adapting Receptors (Eg: Nociceptors):
o Continue to Transmit Impulses to the brain as long as the Stimulus is Applied
• Rapidly-Adapting Receptors (Eg: Pacinian Corpuscles):
o Receptors Rapidly Adapt & are stimulated only when the Stimulus Strength
has Changed
o Connection to the CNS:
§ First Order Neuron:
• Sensory Neuron Nucleus is in the Dorsal Root Ganglion
• Its axon extends from periphery to Dorsal Horn of the Dorsal Root Ganglion
§ Second Order Neuron:
• Neuronal Nucleus is in the Substantia Gelatinosa
• Its axon Decussates, Then it Ascends in the Spinothalamic Tracts → Thalamus
§ Third Order Neuron (Thalamus):
• Neuronal Nucleus is in the Thalamus
• Its axon passes through the Internal Capsule (behind Pyramidal Fibres) → Sensory
Cortex

OpenStax College, CC BY 3.0 <[Link] via Wikimedia Commons

- Glands:
o Sebaceous (Sebum) Glands:
§ Associated with hair follicles (The Pilosebaceous Unit)
• (:. Not found on Palms/Soles)(Most found on Face & Scalp)
§ Holocrine Secretion:
• (Ie: Secretion via complete destruction of cells)
• Produce oily sebum:
o Triglycerides
o Fatty Acids
o Wax Esters
o Cholesterol
o (Also Antibacterial/Antifungal Action)
§ Stimulated by Androgens:
• Stimulated by Androgens (Inhibited by Estrogens)
• Very Active at puberty
o Eccrine (Sweat) Glands:
§ On most of the body (Scarce on the back)
§ Simple, Coiled Tubular Glands:
• Secretory Coil (deep in Dermis) – Secrete the Water & Electrolytes
• Sweat Duct – Reabsorb Na+ Ions from the sweat
§ Clear watery secretion
• Person can perspire several liters per hour
• Process:
o 1) Secretion of Electrolyte-Rich Fluid
o 2) Reabsorption of excess Na+ by the Duct
§ Stimulated by High Temperature and Stress
• Emotional Sweating doesn’t occur during sleep
• Thermal sweating does occur during sleep
• Innervated by Sympathetic Nerves

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

o Apocrine (Pheromone) Glands:
§ Associated with hair follicles
§ Large complex gland:
• Located in Dermis
• Duct Opens into Hair Follicle
§ Viscous, Milky Secretion – (protein and cellular debris):
• Produces pheromones
o Bacterial action is required for odor production
o Thought to have or had a role as a sexual attractant in humans
o Respond to emotive stimuli
§ Stimulated by Androgens:
• Most Active at puberty

Source: [Link]
- Nails (“Ungals”):
o Composition:
§ Plate of hardened and densely packed keratin (Protein)
o Functions:
§ Protect distal phalanges of fingers and toes
§ Aid in picking up objects
§ Efficient natural weapon
o Structural Landmarks:
§ Nail Plate:
• Fully keratinized structure
• Firmly attached to the nail bed
§ Nail Bed: Skin underneath the nail
§ Lunula: Proximal whitish half-moon-shaped area on Nail Plate
§ Cuticle: The dorsal part of the proximal nail fold
§ Nail Matrix: Nail growth occurs From Here - by proliferation and differentiation of the nail
matrix
§ Paronychium: The Skin around the Nail
§ Hyponychium: The area where the nail plate detaches from the digit
§ Proximal Nail Fold: The fold at the Proximal Edge of the nail (Covers ≈1/4 of the nail)
§ Lateral Nail Folds: The folds of skin at the Lateral Edges of the Nail

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

- Hair/The ‘Pilosebaceous Unit’:
o The Pilosebaceous Unit:
§ Hair Shaft
§ + Sebaceous/apocrine ducts empty into hair follicles
o Arrector Pili Muscle:
§ Smooth Muscle
§ Supplied by Adrenergic Nerves
§ → Erection of the Hair during Cold/Emotional Stress (Goose-Bumps)
o 2 Types of Hair:
§ Vellus:
• Fine, Short & Almost invisible
• (All over the body)
§ Terminal:
• Thick, coloured & Visible
• (Scalp, beard, axilla, genital area)
o Hair Follicles Respond to Androgen:
§ Pre-pubertal children don’t have Terminal Hair in Axilla/Genital Area/Facial Hair
§ During Puberty, hair grows in these areas
§ With age, androgen stimulation decreases → Terminal Hair on scalp reverts from Terminal to
Vellus hair (Hair follicles aren’t lost, but change to Vellus hair)
o Hair follicles undergo cycles of Growth, Resting and Shedding:
§ Anagen (growing):
• Lasts 3 Years
• Keratinocytes in the follicular bulb proliferate to form the hair shaft
§ Catagen (Resting):
• Lasts 2 Weeks
• The keratinocytes and melanocytes undergo programmed cell death
§ Telogen (Shedding):
• Last 3 Months
• Hair but does not grow
• May Remain Anchored, or Be Shed
• Following telogen a new growth cycle will begin (Ie: anagen)
o Hair Pigmentation:
§ Colour of hair is determined by the melanocytes – actively pigmented only in Anagen
§ Absence of pigment →white hair
§ Diminished pigment →grey hair

Mechanisms of Healing:
- Acute Inflammation:
o Vasodilation
o Increased Permeability → Stasis
o Leukocyte Margination/Migration
o Phagocytosis of Damaged/Dead Tissue/Organisms + Enzyme Release
- Granulation Tissue:
o 3-5 Days After Injury
o Occurs only in Deeper Cuts/Injuries (Not Superficial Injuries)
o Angiogenesis – (Migration + Proliferation of Endothelial Cells)
§ Driven by FGF (Fibroblast Growth Factor) + VEGF (Vasculo-Endothelial Growth Factor)
o Fibrosis - Fibroblast Migration + Proliferation
§ Driven by PDGF (Platelet-Derived Growth Factor) + TGFB (Transforming Growth Factor-B)
- Collagen Synthesis:
o A Triple Helix Protein
o Synthesis is Vitamin C Dependent
o As time goes by, the Collagen Scar gets Stronger:
§ At 1wk, the scar is weak
§ Strengths peaks @ 3mths
o Metalloproteinases (collagenases, Gelatinases) → Degrade Collagen

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

Healing By Primary Intention Vs Secondary Intention:
- Primary Intention:
o Wound edges are CLOSE together
o Tends to be Quick
o Cells of the Basal Layer of the Epidermis lines the Surface of the Wound (within 1-2 Days)
- Secondary Intention:
o Wide, open wound (Edges are FAR apart)
o Takes a lot Longer
o Granulation Tissue Fills the Wound → Epithelialisation from Wound Margins

Unattributable
GENERAL PRINCIPALS OF DERMATOLOGY

Key words + Definitions:

- Primary Lesion:
o The initial lesion that characterizes a condition
- Secondary Lesion:
o Over time, the primary lesion may continue to develop or be modified by regression/trauma,
producing a “secondary lesion”

Morphology Terminology – Primary Lesions:

Lesion Name: Lesion Description: Picture:

Erythema Redness due to vascular dilation (Eg: Cellulitis)

Erythroderma Red rash covering >90% of the Body

Telangiectasia Permanently dilated dermal blood vessels to the point of

being visible; Blanches under pressure

Macule A macule is a small, flat is of altered colour, without

elevation or depression (nonpalpable). (Eg: Lentigo
Simplex, Eg: Freckles)

Patch A patch is a large Macule

Petechiae Tiny macules of blood in the skin; Small, non-blanching

Extravasated RBC’s

Purpura A Large Macule or Patch of blood in the skin. Doesn’t

(May Be blanch under pressure. (Eg: A Hickey)
Palpable) Larger area of RBC extravasation

(The hallmark of vasculitis – severe inflammation of the

blood vessels; If it is this bad in the skin, it’s probably this
bad elsewhere in the body)
Ecchymosis/ A Larger subcutaneous bleed. The resultant swelling = a
Haematoma ‘Haematoma’

Micropapule A Very Small raised lesion 1-2mm in diameter.

Papule A small raised lesion (less than 0.5cm)

Plaque Flat-topped, raised area of the skin. (Usually dermal

thickening.)
A large Papule more than 2cm in width but NO depth.
(Eg: Psoriasis)

Papilloma A nipple-like mass projecting from the skin

Burrow A linear Papule caused by a burrowing organism. Eg:

Scabies

Nodule A raised, solid lesion greater than 0.5cm in width AND

depth. (Eg: Keloid Scar)

Tumour A mass of enlarged tissues of more than 1cm diameter

Vesicle A clear, fluid-containing elevation of less than 5mm in
diameter. (Eg: Chickenpox)
(Typically appear clear, but can fill with pus to become a
Pustule)

Bulla A large Vesicle more than 0.5cm in diameter

Pustule A small Pus-filled vesicle of less than 5mm in diameter

Impetiginized Covered in Crust, Pustules, & Often Weeping

(Impetigo):

Cyst A cavity containing liquid, semisolid, or solid material

Abscess A Pus-containing cavity of more than 1cm in diameter.

(Note: a cyst can become infected and fill with pus,
becoming an abscess)
Excoriation A Scratch - May be Epidermal or may extend down into
the Dermis
- Often linear
- Often Covered with Crust

Fissure A deep crack - extends down to the dermis & blood

vessels

Erosion A superficial incomplete loss of the epidermis. Eg:

Superficial Burn

Ulcer An area of complete loss of the epidermis and often

portions of the dermis and even subcutaneous fat.

Wheal A wheal is an elevated, white, compressible area

produced by dermal oedema. It typically disappears
within 24 to 48 hours

Angioedema Oedema which extends to the subcutaneous tissue

Comedone A plug of keratin or sebum blocking a sebaceous orifice

(Blackhead)

Alopecia Can be:

(Hair Loss) - Scarring (Permanent loss of hair follicles)
- Or Non-Scarring (follicles are still alive and well)

Eschar Patch of Dead Skin (necrosis) – A Thick Crust over an

(Necrosis) Ulcer or Erosion:
– Typically black; Full-thickness skin loss
(Dead skin = something bad – RED FLAG) (Implies
something vascular → Ischaemic Necrosis)
Morphology Terminology – Secondary Lesions:

Lesion Name: Lesion Description: Picture:

Scale Dry, laminated masses of keratin that represent
thickened stratum corneum. Eg: Psoriasis

Keratosis Thickening of the skin. Eg: Solar Keratosis

Hyperkeratosis Large are of Thickened skin → Thick Scale.

Verrucous Very Hyperkeratotic – Similar to a Wart

Lichenification Palpable epidermal thickening of the skin usually due to

friction. Eg: Lichen Simplex

Crust Dried serum, pus, or blood usually mixed with epithelial

and sometimes bacterial debris

Atrophy Thinning of the skin (epidermal, dermal, or

subcutaneous)
Erosion A superficial incomplete loss of the epidermis. Eg:
Superficial Burn

Ulcer An area of complete loss of the epidermis and often

portions of the dermis and even subcutaneous fat. Eg:
SCC

Excoriation A superficial loss of epidermis from scratching or picking,

therefore often linear and often covered by crust

Scar A pale, firm raised or depressed lesion resulting from skin

injury. Eg: Keloid Scar

Stria Streak-like, linear, pink/purple/white marks due to

(Stretch Marks) changes in Connective Tissue

Pigmentation An Increase or Decrease in skin pigmentation. Eg:

Birthmark
Other Descriptors:
- Colour:
o Erythema = Red
o Violaceous = Purple
o Slate = Gray
o Hyperpigmented = Darker than surrounding skin
o Hypopigmented = Lighter than surrounding skin
o Bronze = Red-Brown
o Dusky = Purple-Grey
o Variegated = Many different Colours

- Relating to Edge of Rash:

o Definition:
§ Eg: Well Defined
§ Eg: Ill/Poorly Defined
o Geometric Shape:
§ Nummular = Round
§ Annular = Rink-like
§ Circinate = Circular
§ Arcuate = Curved
§ Discoid = Disc-like
§ Gyrate/Serpiginous = Wave-like
§ Polycyclic = Edge is like a number of overlapping circles
- Surface Contour:

- Relating to Symptoms:
o Weeping = Oozing clear fluid from the skin surface
o Crusted = Covered in scabs
o Pruritis = Itchy
o Dysaesthesia = Tingling, Burning, Numbness

- Symmetry:
o Eg: Dermatitis is typically symmetrical
o Eg: An infective lesion (Eg: Abscess) is likely to be Unilateral

- Is it in Typical Distribution:
o Eg: Seborrheic Dermatitis (Dandruff) typically occurs on the scalp, forehead, eyebrows & chest
o Eg: Atopic Dermatitis typically in the cubital & popliteal fossae

- Localised or Universal:
o Universal – Eg: Chicken Pox
o Localised – Eg: Herpes Zoster (Shingles) localised to a dermatome
BENIGN CYSTIC SKIN LESIONS
BENIGN CYSTIC SKIN LESIONS

EPIDERMAL CYST
- Clinical Presentation:
o Round, Firm, Mobile
o Slow-growing
o Range from 1cm-several cm across
o May have an enlarged pore in the centre
- Pathophysiology:
o Cystic enclosure of epithelium within the dermis
o → Becomes filled with keratin and lipid-rich debris (Cream coloured/odorous)
o Cyst wall is thin → can rupture → inflammation & pain
- Epidemiology:
o Young-middle age
o Most common type of cyst
- Clinical Course:
o May rupture → inflammation
o May increase in size/number over time
- Management:
o Usually self-limiting
o Can require excision

Public Domain: Serephine, CC0, via Wikimedia Commons

BENIGN FIBROUS SKIN LESIONS
BENIGN FIBROUS SKIN LESIONS

DERMATOFIBROMA
- Aetiology:
• Thought to originate from minor trauma (Eg: Shaving/insect bites)
• Some association with SLE
- Epidemiology:
• Most common in adults
• Most common in females
- Pathophysiology:
• Benign tumour of fibroblast proliferation in Dermis
- Clinical Features:
• Firm Dermal Papule/Nodule
• Skin coloured/darkened
• May be itchy/tender
• Fitzpatrick’s Dimple Sign – lateral compression causes dimpling of lesion
- Management:
• Excision if desired

Jmarchn, CC BY-SA 3.0 <[Link] via Wikimedia Commons

BENIGN HYPERKERATOTIC LESIONS
BENIGN HYPERKERATOTIC LESIONS

SEBORRHEIC KERATOSIS
- Aetiology:
• Totally Benign Tumour in Old Age (Common in >40yrs)
- Pathogenesis:
• Proliferation of keratinocytes & melanocytes → Benign Epithelial tumour
- Morphology:
• Gross:
- Sticky, Oily Plaques
- Round, Flat
- Sharply Defined Borders
- May be Pigmented
- rough, warty surface
- Raised, ‘Stuck-on’ Appearance
• Microscopic:
- Thick Hyperplastic Epidermis
- Keratin Cysts
- Clinical Features:
• Often referred to as "old-age spots"
• Rarely pruritic
• Treated only if inflamed
• No Malignant Potential
- Treatment:
• None required; cryotherapy/excision if desired

James Heilman, MD, CC BY-SA 3.0 <[Link] via Wikimedia Commons

No machine-readable author provided. KGH assumed (based on copyright claims)., CC BY-SA 3.0
<[Link] via Wikimedia Commons
CORNS / ‘HELOMATA’
- Aetiology:
• Pressure
- Epidemiology:
• More common in females
- Pathophysiology:
• Localised hyperkeratosis induced by pressure
- Clinical Features:
• Firm papule with hard keratin core
• Non-innervated but painful with direct pressure
• Common on toes and hands
- Management:
• Relieve pressure (padding/orthotics)
• Paring

Marionette, CC BY-SA 3.0 <[Link] via Wikimedia Commons

BENIGN PIGMENTED LESIONS
BENIGN PIGMENTED LESIONS

CONGENITAL NEVOMELANOCYTIC NEVI (‘BIRTH MARK’)

- Aetiology:
• Congenital
- Pathophysiology:
• Nevomelanocytes in epidermis
- Clinical Features:
• Present at birth
• Rare malignant transformation
- Morphology:
• Well demarcated pigmented papule/plaque
• +/- overlying hairs
• May have surrounding satellite nevi
- Management:
• Take baseline photo and observe for change in shape/colour/size
• Excision if suspicious

Mohammad2018, CC BY-SA 4.0 <[Link] via Wikimedia Commons

ACQUIRED NEVOMELANOCYTIC NEVI (COMMON MOLE)
- Aetiology:
• Thought to be initiated by UV Exposure
• Familial association
- Epidemiology:
• Are normal
- Pathophysiology:
• benign tumours of melanocytes
- Clinical Features:
• Well demarcated, round, pigmented macule
• Uniform pigmentation
• <1)5cm diameter
• Usually Benign (But can become malignant)
- 3 Stages of Evolution:
• Junctional Naevus (Typical Birthmark) = Excess Melanocytes AND Excess Pigment
- Small, Flat, Symmetric, Uniform Lesions
- Cluster of Clear Cells (Melanocytes) @ the Dermo-Epidermal Junction
• Compound Naevus:
- Small, Raised, Dome-Shaped, Symmetric, Uniform Lesions
- Big Clusters of Melanocytes in Dermis & Dermo-Epidermal Junction
• Dermal:
- Dome-shaped papule/nodule
- Melanocytes are exclusively in the Dermis
- Management:
• New/evolving lesions should be evaluated for melanoma
• Consider Excisional biopsy if Asymmetric/non-uniform colours/irregular borders/itch/bleeding

Buckley D. (2021) Congenital Nevi, Melanocytic Naevi (Moles) and Vascular Tumours in Newborns and Children. In:
Buckley D., Pasquali P. (eds) Textbook of Primary Care Dermatology. Springer, Cham. [Link]
030-29101-3_29
ATYPICAL NEVUS (DYSPLASTIC NEVUS)
- Aetiology:
• UV exposure
• Progression of a pre-existing common mole
- Epidemiology:
• Family history
• High number of common moles
- Pathophysiology:
• DermoEpidermal-Junctional Cluster of Dysplastic (Larger/Irregular/Darker) Melanocytes
• Clinically and histologically as intermediates between normal naevi and melanoma
• Small risk of transformation to melanoma (about 1 in 1000)
- Clinical Features:
• Pigmented, Raised Lesion, with Central Darker Shade
• Macular & Papular
• Uneven pigmentation
• Fairly regular borders
• Fair symmetry
- Management:
• Baseline photography/monitoring
• Excisional biopsy

Source: [Link]
EPHELIDES (FRECKLES)
- Aetiology:
• Sun exposure
- Epidemiology:
• Most common in fair-skinned people (Fitzpatrick 1 & 2 skin types)
• Appear in childhood
- Pathophysiology:
• UV Exposure → Increased melanin within basal layer keratinocytes
- Clinical Features:
• Small <5mm well-defined light brown macule
• May Regress if Exposure is Avoided
- Management:
• Sun-safe practices (cover skin/sunscreen)

Loyna, CC BY-SA 2)5 <[Link] via Wikimedia Commons

SOLAR LENTIGO
• Aetiology:
o UV-Exposure
• Epidemiology:
o common in middle aged to elderly fair skinned people
• Pathophysiology:
o Benign melanocytic proliferation in dermal-epidermal junction due to chronic sun exposure
• Clinical Features:
o brown, well-defined macules on sun exposed skin
o 1-3cm diameter
• Management:
o Laser therapy
o Shave excision
o Cryotherapy

Alain Gérard, CC BY-SA 4.0 <[Link] via Wikimedia Commons

VASCULAR LESIONS
VASCULAR LESIONS

HAEMANGIOMAS
- Aetiology:
• congenital
- Epidemiology:
• Appears shortly after birth
- Pathophysiology:
• Benign vascular tumour
- Clinical Features:
• Approx half resolve spontaneously by around 5yrs
• Red/blue subcutaneous mass
• Soft/compressible
• Blanches with pressure
- Management:
• Consider treatment if not gone by school age
- Topical Timolol
- Propanolol
- Corticosteroids
- Laser treatment
- surgery

Source: [Link]
PORT-WINE STAINS
- Aetiology:
• Congenital
- Epidemiology:
• Present at birth
• Rarely associated with Sturge-Weber syndrome
- Pathophysiology:
• Vascular malformation of dermal capillaries
- Clinical Features:
• Red-blue macule
• Follows a dermatomal distribution
• Rarely crosses midline
• Commonly on nape of neck
• Doesn’t spontaneously regress
- Management:
• Laser therapy

Bin im Garten, CC BY-SA 3.0 <[Link] via Wikimedia Commons

ACNEIFORM ERUPTIONS:
ACNEIFORM ERUPTIONS:

ACNE VULGARIS (COMMON ACNE)

- Aetiology & Pathogenesis:
o Genetic Basis (Familial)
§ Chronic inflammation of the sebaceous glands
o Abnormalities of the Pilosebaceous Unit:
§ Blockage of the Sebaceous Duct (By ↑Keratin @ Duct Opening)
§ Increased Sebum Production (Often under influence of ↑Androgen)
§ → Bacterial Infection of the Pilosebaceous Unit (Propionibacterium Acnes)
§ → Rupture of the Sebaceous Duct
§ → Inflammatory Effects
o Note: Combined Oral Contraceptives (Ie: With Progesterone) can contribute to Acne
o (IF Severe, Damage to Dermis Occurs → Scarring. Note: Scarring is a FAILURE of the Doctor to
Adequately treat Acne)
- Epidemiology:
o Common Skin Condition in Teenagers (Although Can occur at any age)
o Most Severe in Males
- Presentation:
o Wide Variation in Severity
o Most often on Face, Upper Chest & Back
o **Presence of Comedones – Both Open (Blackheads) & Closed (Whiteheads)
§ (Note: If no comedones are present, consider Differential Diagnoses)
o Inflammatory Papules & Pustules
o Severe Cases →
§ Cysts
§ Scarring (Hypertrophic or Atrophic)
- Diagnosis:
o The ‘Acne Triad’:
§ Papules + Pustules + Comedones = ACNE
o Possible Differential Diagnoses:
§ *Rosacea:
- Treatment:
o Topical Anti-inflammatories & Antiseptics
o Antiseptics (Eg: Benzoyl Peroxide)
o Antibiotics (If Severe)(Note: Tetracycline also has an Anti-Inflammatory Effect – Good)
o Keratolytics (To ↓the overproduction of keratin – Eg: Salicylic acid)
o Retinoids (Derived from Vitamin A) (Isotretinoin/Roaccutane) (In Severe Nodulo-Cystic Acne)
o ≈1yr after symptoms disappear
- Prognosis:
o Usually Good (Most cases are Self-Limiting)
o Treatments are safe & well-tolerated
o NO Patient should have to Suffer!
Roshu Bangal, CC BY-SA 4.0 <[Link] via Wikimedia Commons

Source: Unattributable
ROSACEA
- What is it?:
o Predominantly a Facial Rash easily confused with Acne
o = Pustules and Papular Rash on Face
o Typically a Disease of Middle Age (30-40yrs)
- Aetiology:
o Unknown
o (But Familial Association)
o Aggregating Factors:
§ Heat and steam
§ Hot, spicy food
§ Alcohol consumption
§ Emotional stress
§ Sun exposure
- Presentation:
o Wide Variation in Severity
o Initial Signs:
§ Tendency to Flush easily + Burning/Stinging/Itching
o Distinguishing Features:
§ Facial Flushing (Erythema)
§ Dilated, visible Capillaries (Telangiectasia)
§ Papules
§ Pustules
§ But NOT Comedones
o If Severe:
§ Disfiguring Facial Rash
§ + Bulbous Enlargement of the Nose
§ Possible Facial Oedema
o NO Comedones (:. NOT Acne)
o Does not cause Scarring
o Very Chronic (Not Self Limiting – May last for many years)
o (Note: Often significant Psychosocial Impact – Eg: Depression)
- Diagnosis:
o Differential Diagnoses:
§ Acne (has all features + Comedones)
§ Sun Damage (has Telangiectasia, but No other Features)
§ Lupus Erythematosus (Have Telangiectasia & Erythema, But NO Pustules or Papules)
§ Menopause (Flushing)
- Treatment:
o Avoidance of Aggravating Factors
o Similar Treatment to Acne
§ Antibiotics (Some have Anti-Inflammatory Effects)
§ Retinoids
o Laser surgery (for Telangiectasia & Erythema)
o Topical corticosteroids make rosacea worse and should never be used to treat it!
§ → Cause Perioral Dermatitis (Should NEVER be used in Rosacea)
Source: [Link]
DERMATITIS (ECZEMA)
DERMATITIS (ECZEMA)

ACUTE DERMATITIS/ECZEMA:
- Types of Acute Eczema:
o CONTACT DERMATITIS (Due to prolonged exposure to allergen)
o ATOPIC DERMATITIS
o (Drug eczema)
o (Photoeczema)
o (Primary irritant dermatitis)
- Aetiology:
o Type IV Hypersensitivity (T-Cell Mediated) to Allergen
o Prolonged Contact with Allergen - Urine, Soaps, Antiseptics, Deodorants, Creams, Foreign Body, etc
- Epidemiology:
o Family history – (in 70% of cases)
o Most Common in Children
o Genetics – (50% of pts have a deficiency of the Epidermal Protein “Filaggrin” )
o Hypersensitivity – (Associated with other Atopies (Hay Fever [Allergic Rhinitis], and Asthma))
- Pathogenesis:
o Initial Exposure:
§ Ag Processed by Langerhans Cells →Presented to T-Cells in LN → T-Cell Activation
o Re-Exposure:
§ Type IV Hypersensitivity (T-Cell Mediated) reaction to Allergen
§ → Epidermal Oedema + Small Blisters → “Wet Eczema”
o Chronic Exposure:
§ →Hyperplasia, hyperkeratosis (lichenification) – “Dry Eczema”
- Morphology:
o Gross:
§ Erythema
§ Small Blisters – (Weeping & Crusting Blisters, Papules and Plaques )
§ Hyperkeratosis (If Chronic)
o Microscopic:
§ Intra-Epidermal Oedema (Spongiosis)
§ Epidermal Blistering
§ Perivascular Inflammatory Infiltrate
- Clinical Features:
o Severe Itching
o Patchy, Erythematous, Poorly Defined Rash
§ Usually in the Popliteal/Cubital Fossae & Face
§ Can be Generalised
o Dry Skin
o Excoriation (loss of the surface of the skin from scratching) due to itching and scratching
o Lichenification (thickening of the skin with accentuated skin lines)
o Crusting (scabbing) and weeping (loss of fluid through the surface of the skin) due to bacterial
infection
o (Contact dermatitis often has a regular shape (Eg: Square from Band-Aid))
- Treatment:
o Modification of lifestyle to avoid exacerbating factors
o Remove Allergen
o Avoid Soaps
o Use of moisturisers and bath additives
o Treated with topical Corticosteroids (Symptomatic)
o Antihistamines (For Itch)
Source: [Link]

James Heilman, MD, CC BY-SA 4.0 <[Link] via Wikimedia Commons

OpenStax College, CC BY 3.0 <[Link] via Wikimedia Commons
SEBORRHEIC DERMATITIS
• Aetiology:
o Some heredity
o Some association with commensal Malassezia yeast (fatty acid metabolites may cause inflammatory
reaction)
• Risk Factors:
o Oily skin
o Familial history of dermatitis/psoriasis
o Immunosuppression
o Parkinson’s disease
o Sleep deprivation/stress
• Epidemiology:
o Bimodal onset; Infancy (within the first months), or between 20-50yrs old
o Most common in males
• Pathophysiology:
o Not completely known
• Clinical Features:
o Chronic/relapsing eczema (improves in summer; flares in winter)
o Primarily affects sebaceous-rich regions (Scalp/face/trunk)
o Ill-defined, localised scaly patches/scale
o Blepharitis (scaly red eyelid margins)
o Salmon-pink thin scaly and ill-defined plaques in skin folds
o Infantile Seborrheic Dermatitis:
§ Numerous Dermatoses in the 1st 3 Months of Life
§ Erythematous but Non-Itchy Rash involving the face, scalp, neck, axillae and nappy area. The
lesions are well defined and covered in greasy scale
o Adult Seborrheic Dermatitis:
§ Erythema and fine, greasy scale on the cheeks, nose and nasolabial folds
§ Scale and itching of the scalp and eyebrows
§ Well defined but non-scaly erythema of the axillae, groin, scrotum and perianal skin
• Management:
o Keratolytics (Eg: Salicylic Acid)
o Topical antifungals (Eg: Ketoconazole)
o Mild topical steroids
o (Isotretinoin for moderate/severe seborrheic dermatitis)

Amras666, CC BY-SA 3.0 <[Link] via Wikimedia Commons

Roymishali, CC BY-SA 3.0 <[Link] via Wikimedia Commons
STASIS DERMATITIS (VENOUS ECZEMA)
- Aetiology:
• Venous insufficiency + Gravity
- Epidemiology:
• Middle-older-aged patients
• 20% of over 70yr olds
• Risk factors:
- History of DVT in affected limb
- Varicose veins
- Venous leg ulcers
- Pathophysiology:
• Venous insufficiency → Failure of calf pump mechanism
• → blood pools in leg veins → increased venous hydrostatic pressure → oedema
• Fluid collecting in tissues → Activation of innate immune response
- Clinical Features:
• May form discrete patches or become confluent/circumferential
• Itchy red, blistered & crusted plaques
• On one or both lower legs
• Orange-brown macular pigmentation due to Haemosiderin deposition
• Champagne bottle shape of lower leg
- Management:
• Reduce Dependent Oedema:
- Elevate feet when sitting
- Walk regularly
- Elevate feet above bed level overnight
- Graduated compressing stockings long-term
• Treat Eczema:
- Dry up oozing patches with potassium permanganate or dilute vinegar on gauze compress
- Oral antibiotics to avoid secondary infection
- Topical steroid
- Moisturising cream
- Avoid injury to skin
• Treat Varicose Veins:
- Consult vascular surgeon
- Sclerotherapy/laser

James Heilman, MD, CC BY-SA 4.0 <[Link] via Wikimedia Commons

LICHEN SIMPLEX CHRONICUS
- Aetiology:
• Repetitive scratching and rubbing, which arises because of chronic localised itch. The primary itch
can be due to:
- Atopic Eczema
- Contact eczema
- Venous eczema
- Psoriasis
- Lichen planus
- Fungal infection
- Epidemiology:
• Males and females
• Unusual in children
• Association with anxiety/OCD
- Pathophysiology:
• Repetitive scratching/rubbing → hyperkeratosis & inflammation
- Clinical Features:
• Chronic, lichenified eczema/dermatitis
• May be single or multiple plaques
• Dry/scaly surface
• Leathery induration
• Scratch marks
- Management:
• Potent topical steroids 4-6wks until plaque is resolved
• Coal tar preparations
• Moisturisers
• Antihistamines for itch
• Antidepressant for psychosomatic aetiologies

Eyon, CC BY-SA 3.0 <[Link] via Wikimedia Commons

Eyon, CC BY-SA 3.0 <[Link] via Wikimedia Commons
ERYTHEMA MULTIFORME:
- Aetiology:
o Hypersensitivity reaction
o Some genetic tissue-type associations (HLA-B15, -B35, -A33, -DR53, -DQB1*0301)
- Pathogenesis:
o Hypersensitivity Response to:
§ Infections (Herpes simplex, Mycoplasma) *Most common
§ Drugs (Sulphonamides, penicillin, barbiturates)
§ Malignancy (Carcinoma, lymphoma)
§ Auto-Immune (Eg: Lupus, SS, Dermatomyositis)
- Morphology:
o Gross:
§ Variable Lesions: Papules/Plaques/Nodules/Blisters/Ulcers
§ Characteristic “Targetoid” Lesions
• Central Grey Necrosis
• Erythematous raised border
o Microscopic:
§ Dyskeratosis
§ Necrotic Keratinocytes
§ Spongiosis (Epidermal Oedema)
§ Epidermal Lymphocytes
§ Destruction of Basal Epidermal Layer
- Clinical Features:
o Acute & Self-limiting
o Commonly affects young adults (20-40yrs)

Grook Da Oger, CC BY-SA 3.0 <[Link] via Wikimedia Commons

James Heilman, MD, CC BY-SA 3.0 <[Link] via Wikimedia Commons

Source: Unattributable
PAPULOSQUAMOUS DISEASES
PAPULOSQUAMOUS DISEASES

LICHEN PLANUS:
- Aetiology:
o Genetic predisposition
o Physical/emotional stress
o Localised skin disease (Eg: Herpes zoster)
o Systemic viral infection (Eg: Hep C)
o Contact allergy
o
- Pathogenesis:
o Chronic inflammatory skin condition
o Similar to Erythema Multiforme (Hypersensitivity), but more chronic
- Morphology:
o Gross:
§ Purple, polygonal, planar, Papules & Plaques
o Microscopic:
§ Anucleate Dead Cells in Basal Layer (“Civatte Bodies”)
§ Hyperplasia
§ Hyperkeratosis (Scaling)
- Clinical Features:
o Itchy, Purple Polygonal Papules/Plaques
o Shiny, flat-topped and firm on palpation
o on Skin (commonly wrists & ankles), Mucosa, Genitals, Oral
o Self-limiting (1-2 yrs)
- May affect skin and mucosal surfaces; Several clinical types:
o Cutaneous lichen planus
o Mucosal lichen planus
o Lichen planopilaris
o Lichen planus of the nails
o Lichen planus pigmentosus
o Lichenoid drug eruption

James Heilman, MD, CC BY-SA 3.0 <[Link] via Wikimedia Commons

PITYRIASIS ROSEA
- Aetiology:
• Viral infection
- Epidemiology:
• Mostly teenagers & young adults
- Pathophysiology:
• Associated with reactivation of HHV6/7 (which cause roseola in infants)
- → Influenza viruses & vaccines can also trigger pityriasis rosea
- Clinical Features:
• Post-viral rash that occurs several days after an URTI (cough/cold/sore throat etc)
• lasts 6-12 weeks
• Characterised by a ‘herald patch’ followed by similar smaller oval red patches on chest and back
• Herald patch:
- Appears 1-20 days before generalised rash
- Oval pink/red plaque
- 2-5cm diameter
- scale
• Secondary Rash:
- Appears a few days after the herald patch
- More scaly patches/plaques
- Mostly on chest and back
- Some on thighs/upper arms/neck
- Management:
• Bathe/shower with plain water & bath oil/aqueous cream/other soap substitute
• Apply moisturisers
• Some sun exposure
• May treat with acyclovir
• Topical steroid cream may reduce itch
• Phototherapy

[Link]
PSORIASIS
- Aetiology:
o Multifactorial (Genetic & Immune-mediated inflammatory disorder)
o Emotional stress and physical trauma both exacerbate and precipitate psoriasis
- Pathogenesis:
o Important role of T-cell immunity is recognised
o Sensitized T cells infiltrate the skin and secrete cytokines and growth factors
§ →Continuous stimulation of basal cells → Increased cell turnover
§ + →Inflammation, Vascular Proliferation Angiogenesis
- Morphology:
o Gross:
§ Plaque covered with Silvery Scales (Due to Hyperkeratosis & Parakeratosis)
• Bilateral
• Well-Demarcated plaques (Differentiates it from Dermatitis)
• Erythematous Based
§ Abnormalities of the Nails (Dystrophy/Pitting/Onycholysis)
§ Auspitz Sign - Microbleeding when crusts are removed
o Microscopic:
§ Acanthosis (Deepening of Rete Ridges & Thickening of the Epidermis)
§ Parakeratosis (Stratum Corneum still has Nuclei)
§ Neutrophilic Microabscesses in the Epidermis
§ Tortuous Papillary Dermal Vessels

- Clinical Features:
o Psoriasis may present at any age from infancy onwards
o Generally persists lifelong; fluctuating in extent & severity
o NOT itchy
o Symmetrical distribution
o Can cause Multi-System Disorder:
§ Psoriatic Arthritis
§ Myopathy
§ Enteropathy
§ Immunodeficiency
- Diagnosis:
o Clinical diagnosis made on the basis of morphology
o Punch biopsy can be definitive
- Treatment:
o Emollients
o Coal tar preparations
o Dithranol
o Salicylic acid
o Vitamin D Analogue (Calcipotriol)
o Topical CorticoSteroids
o Sunshine/Phototherapy
o (Systemic if severe: Eg: Methotrexate/Ciclosporin/Acitretin)
- Prognosis:
o Chronic
o NOT Curable
o Can be exacerbated by Stress
Haley Otman, CC BY 3.0 <[Link] via Wikimedia Commons

CopperKettle, CC BY-SA 3.0 <[Link] via Wikimedia Commons

Scientific Figure on ResearchGate. Available from: [Link]

section-100-demonstrating-classic-findings-of-psoriasis_fig1_333137128
VESICULOBULLOUS DISEASES
VESICULOBULLOUS DISEASES

BULLOUS PEMPHIGOID
- Aetiology:
o Autoimmune subepidermal blistering disease
o Some association with psoriasis, malignancy, HLA (Human leukocyte antigen)
o Can be associated with PD1-Inhibitor-Immunotherapies (Eg: Pembrolizumab, nivolumab) used to
treat metastatic melanoma
- Epidemiology:
o Old Age Patients (Usually >80yrs)
o M=F
- Pathogenesis:
o Antibody against Basal Layer → Inflammation → Destroys Sub-Epidermal Anchoring Proteins
o Dissociation of the dermal-epidermal layer → Blisters
- Morphology:
o Gross:
§ Separation of the whole epidermis from the dermis
§ Large, Tense, Subepidermal Bullae
§ Sometimes Haemorrhagic Blisters
o Microscopic:
§ NO Acantholysis
- Clinical Features:
o Non-specific rash for several weeks before blisters appear
o Eczematous areas
o Urticaria-like red skin
o Appearance of fluid filled blisters (clear or cloudy, yellowish/bloodstained fluid)
- Complications:
o Staphylococcal/streptococcal skin infection → Sepsis
- Treatment:
o Ultra-potent topical steroids for localised disease
o Systemic steroids (Eg: Prednisone) for generalised disease
o Tetracycline antibiotics (Eg: Doxycycline) may be effective as monotherapy for very mild disease
o Antibiotics for secondary bacterial infection
Mohammad2018, CC BY-SA 4.0 <[Link] via Wikimedia Commons

Subepidermal blistering [solid arrows in (A,B)] and influx of inflammatory cells including eosinophils and
neutrophils in the dermis [solid arrow (C)] and blister cavity [dashed arrows (C)]. In (C) also deposition of fibrin is
noted (asterisks).

Jenny Giang, Marc A. J. Seelen, Martijn B. A. van Doorn, Robert Rissmann,Errol P. Prens and Jeffrey Damman, CC BY
4.0 <[Link] via Wikimedia Commons
PEMPHIGUS VULGARIS
- Aetiology:
o Autoimmune
o May also be drug-induced (Eg: Penicillamine, ACE-inhibitors, ARB’s, & Cephalosporins)
- Epidemiology:
o Onset 30-60yrs
o More common in Jewish and Indian descent (genetic association)
- Pathogenesis:
o Antibodies against Desmosomes (that hold keratinocytes together)→ Destroys Desmosomes
o Keratinocytes separate from each other → Acantholysis (Intraepidermal Blisters)
- Morphology:
o Gross:
§ Thin, Flaccid Blisters (Easily Popped)
§ Look similar to burns
§ Many have popped → Crusting
o Microscopic:
§ Acantholysis (Intraepidermal Bullae)
§ Loose cells inside the Bullae
- Clinical Features:
o Common on mucous membranes (Eg: Mouth/genitals)
o Blisters typically develop after a few weeks/months
o Popped blisters lead to itchy, painful erosions
- Treatment:
o Systemic corticosteroids (moderate to high dose oral prednisone/prednisolone)
§ Or pulsed IV methylprednisolone
o Other immunosuppressants (Eg: Azathioprine/Cyclophosphamide/Rituximab)
- Complications:
o Secondary bacterial infection
o Secondary fungal infection (Eg: Candida)
o Viral infections (Eg: Herpes simplex)
o Complications of long term corticosteroid use

Mohammad2018, CC BY-SA 4.0 <[Link] via Wikimedia Commons

Nephron, CC BY-SA 3.0 <[Link] via Wikimedia Commons

Microscopic image of direct immunofluorescence using an anti-IgG antibody.

Emmanuelm at English Wikipedia, CC BY 3.0 <[Link] via Wikimedia

Commons
DERMATITIS HERPETIFORMIS
- Aetiology:
o Associated with Coeliac Disease (Gluten Sensitivity)
o (Note: ‘Herpetiformis’ is a misnomer derived from the tendency for blisters to appear in clusters,
similar to herpes simplex)
- Epidemiology:
o Caucasians age 15-40yrs
o M:F = 2:1
o Genetic association with HLA (human leukocyte antigens)
o Occurs in 15-25% of coeliac patients
- Pathogenesis:
o Gluten triggers IgA antibodies in an autoimmune process that targets the skin and gut →
Inflammation
- Morphology:
o Gross:
§ VERY Itchy, Small, Erythematous Papules
§ Vesicles
§ Occasional Bullae
o Microscopic:
§ Subepithelial, Neutrophilic Microabscesses in Dermal Papilla
- Clinical Features:
o Associated with Coeliac Disease
o Symmetrical distribution
o Commonly on scalp/shoulders/buttocks/knees
o Lesions often resolve to leave hypopigmentation or hyperpigmentation
- Treatment:
o Gluten free diet
o Medication:
§ Dapsone (Gold standard)
§ Otherwise topical steroids/systemic steroids/sulfapyridine/Rituximab if intolerant to
Dapsone

Madhero88, CC BY-SA 3.0 <[Link] via Wikimedia Commons

Subepidermal vesicles, with papillary neutrophil microabcesses, with neutrophil, eosinophil and lymphocytes
infiltrates in the superficial dermis

Beatriz Di Martino Ortiz, Hugo Macchi, Celeste Valiente Rebull, María Lorena Re Dominguez, Guadalupe Barboza, CC
BY 4.0 <[Link] via Wikimedia Commons
PORPHYRIA CUTANEA TARDA
- Aetiology:
• Genetic or acquired defect in Liver enzyme ‘uroporphyrinogen decarboxylase’ (UROD)
- 30% of patients are hereditary
- Other patients, cause is underlying liver disease (Eg: Alcoholism, hep B/C, hemochromatosis)
- Dialysis patients also at risk as cannot excrete porphyrins
- Epidemiology:
• The most common type of porphyria
- Pathophysiology:
• A deficiency or block of one of the enzymes in the porphyrin pathway of haem synthesis → results in
a build-up of precursor protein or intermediate molecule
- Clinical Features:
• Photosensitivity
• Increasingly fragile skin on back of hands/forearms
• Other sun-exposed areas (Eg: Face/scalp/neck) may also be affected
• Slow-to-heal crusted erosions following minor injuries
• Fluid/blood-filled blisters
• Post inflammatory pigmentations & milia
• Characteristically dark reddish/tea-coloured urine
- Management:
• Reduce alcohol consumption
• Cease oestrogen/HRT
• Avoid excessive iron intake
• Hep C treatment (If relevant)
• Sun-protective clothing
• Venesection (approx 500mL of blood every 2-4 weeks) to reduce iron stores to normal
• Hydroxychloroquine can be useful in elderly/anaemic patients; aids porphyrin excretion

Creative Commons Attribution 4.0 International License:

[Link]
Change in urine colour before and after sun exposure Left figure is urine of the first day. Right figure is urine after sun
exposure for 3 days. Urine colour changed to “port wine” colour after sun exposure. This colour change is due to
increased concentrations of porphyrin intermediates in the urine, indicating an abnormality in production and a
partial block within the enzymatic porphyrin chain with metabolite formation. The urine colour usually becomes
darker with acute illness, even dark reddish or brown after sun exposure.

Chen GL, Yang DH, Wu JY, Kuo CW, Hsu WH, CC BY 3.0 <[Link] via
Wikimedia Commons
DRUG ERUPTIONS
DRUG ERUPTIONS

MORBILLIFORM DRUG REACTIONS

- Aetiology:
• Type IV Hypersensitivity
• (Typically caused by antibiotics)
- Epidemiology:
• Most common type of drug reaction
- Pathophysiology:
• Allergic reaction mediated by Cytotoxic T-Cells → Cytokines → Inflammation
- Clinical Features:
• Maculopapular exanthema
- Typically on trunk → limbs & neck
- Bilateral & symmetrical
- Annular, targetoid, urticarial-like or polymorphous lesions
• Typically 1-2 weeks after starting a drug & up to 1wk after stopping it
• More rapid drug eruption to subsequent exposure
- Management:
• Identify causative drug and stop it!
• Monitor for complications
• Emollients
• Potent topical steroid creams
• Antihistamines have some limited benefit

Credit: [Link]
URTICARIAL DRUG REACTIONS
- Aetiology:
o Type I hypersensitivity – Allergy (Food/drug/plant/etc)
- Pathogenesis:
o Antigen is Re-Exposed to a sensitized Mast-Cell/Basophil → IgE-Bound Mast Cell Degranulates:
§ → Releasing Inflammatory Mediators (Histamine) of Type-1-Hypersensitivity Reactions
§ →Perivascular inflammatory infiltrate: lymphocytes, neutrophils or eosinophils
- Morphology:
o Gross:
§ Erythematous Papules & Plaques (Reddish, raised areas)
o Microscopic:
§ 1) Dermal Oedema (Not Spongiosis – which is Epidermal Oedema)
§ 2) Dilated Dermal Blood Vessels (With Perivascular Inflammatory Cells)
§ 3) Dermal Inflammatory Infiltrate (Lymphocytes, Neutrophils, Eosinophils)
§ (Normal Epidermis – No Spongiosis or Hyperplasia)
- Clinical Features:
o Usually on trunk and extremities
o Individual lesions are transient, usually resolve in 24 hr, but entire episode may last for days
o All ages, more in 20 – 40y
- Management:
o Stop causative drug
o Cold pack or wet cold compresses may provide relief
o Antihistamine (Eg: Cetirizine / Loratadine / Desloratadine / Fexofenadine)
o Systemic short course prednisone/prednisolone if antihistamines fail
o IM Adrenaline if threatened anaphylaxis or throat swelling

James Heilman, MD, CC BY-SA 3.0 <[Link] via Wikimedia Commons

HERITABLE DERMATOSIS
HERITABLE DERMATOSIS

ICHTHYOSIS VULGARIS
- Aetiology:
• Inherited or acquired
• (Autosomal semidominant if inherited)
• Loss-of-function mutations in the gene encoding for protein Filaggrin (FLG)
- Epidemiology:
• The most common form of inherited ichthyoses
• Most common in Europeans
- Pathophysiology:
• Defective production of Filaggrin (which normally binds keratin fibres in epidermal cells to form an
effective skin barrier)
• → Defective skin barrier → excess trans-epidermal water loss → Xerosis (dryness)
• → Excessive scale → hyperkeratosis
- Clinical Features:
• Excessive dry, scaly skin
• Symptoms worse in cold/dry climates
• Typically occurs around 2mths after birth
• Symptoms may worsen until puberty
• Xerosis worse on extensor surfaces/scalp/face/trunk; skin folds usually spared
- Management:
• Emollients with high lipid content (Eg: Lanolin cream)
• Bathe in salt water
• Creams or lotions with salicylic acid
• Oral Retinoids (Eg: Isotretinoin) if severe

Gzzz, CC BY-SA 4.0 <[Link] via Wikimedia Commons

NEUROFIBROMATOSIS 1
- Aetiology:
• Autosomal Dominant Inherited
• Or Acquired mutation
- Epidemiology:
• 1 in 3000 births
- Pathophysiology:
• Mutation in the Neurofibromin gene (Chromosome 17)
- Clinical Features:
• 6 or more café-au-lait macules (flat light brown birthmarks)
• Freckling in skin folds
• Lisch nodules in the iris of the eye
• Multiple neurofibromas (tumours hanging off the skin):
- Circumscribed, superficial, soft button-like brown/pink coloured nodules
- Pathognomonic buttonhole invagination when pressed with a finger
• Malformation of long bones & scoliosis
• Short stature/growth hormone deficiency
• Learning difficulties
• Tumours on the optic nerve → visual loss
• Hearing defects
- Management:
• No cure
• Elective excision of problematic lesions
• Risk of isolation/loneliness

T Gnaevus Faber, CC BY-SA 3.0 <[Link] via Wikimedia Commons

Klaus D. Peter, Wiehl, Germany, CC BY 3.0 DE <[Link] via

Wikimedia Commons
VITILIGO
- Aetiology:
• Systemic autoimmune disorder involving the TYR (Tyrosinase) enzyme in melanocytes
- Epidemiology:
• 0.5-1% of the population
- Pathophysiology:
• Depigmenting process due to loss of melanocytes
- Clinical Features:
• Well-defined milky-white patches of skin (leukoderma)
• Pigment loss commonly begins before age 20
• Higher risk of autoimmune conditions (Eg: Diabetes, thyroid disease, pernicious anaemia, Addison’s
disease, SLE, rheumatoid arthritis, psoriasis, etc)
- Management:
• Minimise skin injury
• Cosmetic camouflage (Eg: Make-up/tans/tattooing)
• Sun protection
• Corticosteroid creams
• Experimental use of Ruxolitinib for facial vitiligo
• Phototherapy
• Systemic (Eg: Oral steroids / methotrexate / Ciclosporin / minocycline)
• Depigmentation therapy in severely affected dark-skinned individuals

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

BACTERIAL INFECTIONS
BACTERIAL INFECTIONS

IMPETIGO (SCHOOL SORES)

- What is it?
o Superficial Bacterial Skin Infection
o Most Common in school kids
o Very Contagious – (Spread by Close Contact & Poor Hygiene)
o Usually resolves slowly
- Organism:
o Mostly Staphylococcus Aureus
o Sometimes Streptococcus Pyogenes
§ Can lead to Glomerulonephritis or Rheumatic Fever if it’s Strep
o Staphylococcus Aureus (Bullous) - (Pic 1)
o Streptococcus (Non-bullous) – (Pic 2)
- Presentations:
o Occur most commonly on face
o Fragile vesicles rupture & crust
o Can be confused with HSV
o 1) Nonbullous/Crusted Impetigo:
§ (Most common)
§ Yellow crusts and erosions
§ Itchy/Irritating (but not painful)
o 2) Bullous impetigo:
§ Always due to Staph-Aureus
§ →Mildly irritating blisters that erode rapidly leaving a brown crust
o 3) Ulcerative lesions:
§ Always due to S-Pyogenes
§ Most common in Aboriginal Communities
- Very Infectious
o Epidemic in young children
o Transmitted through skin contact
o Outbreaks associated with poor hygiene / crowded living conditions
- Treatment:
o Cover Affected Areas
o Abstain from School
o Systemic or Topical Antibiotics

James Heilman, MD, CC BY-SA 4.0 <[Link] via Wikimedia Commons

Evanherk at Dutch Wikipedia, CC BY-SA 3.0 <[Link] via Wikimedia
Commons
ERYSIPELAS
- Aetiology:
o Group A Strep (GAS) / Staphylococcus Aureus
o Breaks in skin (Eg: Insect bites/ulcers/cracking skin conditions/eczema)
- Epidemiology:
o Mostly infants & older people
- Pathophysiology:
o Potentially serious bacterial infection of the skin
o → Infection of the upper dermis → extends to superficial cutaneous lymphatics
- Clinical Features:
o A superficial form of Cellulitis
o ‘St Anthony’s fire’ = Intense rash associated with erysipelas
o Rapid onset fevers, chills, rash
o Affected skin has sharp, raised border
o Bright red, firm & swollen
o May blister or become necrotic
o may spread to deeper lymphatics (lymphangitis)
- Management:
o Wound care
o Oral/IV penicillin antibiotic
o Erythromycin/Roxithromycin if Penicillin allergic
o Vancomycin if MRSA

CDC/Dr. Thomas F. Sellers/Emory University, Public domain, via Wikimedia Commons

CELLULITIS
- What is it?
o Bacterial infection of the Dermis and Sub-Cutaneous Tissues
- Organism:
o Adults: 90% due to Staphylococcus Aureus/GAS
o Children: H-Influenzae B
o Associated with cat/dog bite: Pasturella multocida
- Presentation:
o Painful, raised and Oedematous Erythema (Most commonly on Lower Leg)
o Possible Blistering
o Lymphadenopathy - & Malaise & Fever
o Note: Orbital Cellulitis is a medical emergency!
- Distribution:
o Children – Periorbital Area
o Adults – Lower Legs
- There’s typically an underlying cause:
o Lymphedema
o Tinea, Herpes simplex infection, Chronic sinus infection
o Chronic dermatitis
o Poor lower leg circulation
o Wounds
- Treatment:
o Oral/IV penicillin antibiotic
o Erythromycin/Roxithromycin if Penicillin allergic
o Vancomycin if MRSA

Source: [Link]
FOLLICULITIS
- Aetiology:
o Acute pustular infection/inflammation of a hair follicle
o Commonly after Waxing/Shaving
o Commonly Staphylococcus Aureus; may also be caused by yeasts
- Pathophysiology:
o Inflammation of hair follicle/s from any of many causes
- Clinical Features:
o An Erythematous Pustule centred on a Hair Follicle
- Management:
o Careful hygiene
o Appropriate antimicrobials (Eg: Antibiotics if bacterial/Antifungals if fungal)
o Avoid close shaving/discard old razors

Lforlav, CC BY-SA 3.0 <[Link] via Wikimedia Commons

Da pacem Domine, CC0, via Wikimedia Commons

FURUNCLES (BOILS) & CARBUNCLES
- Aetiology:
• Deep form of bacterial folliculitis
• Typically staphylococcus aureus
- Pathophysiology:
• Begin as superficial infections of hair follicles (folliculitis)
- →Organisms travel down Hair Follicles following Disruption (Eg: After Shaving)
- →Development of boils (furuncles)
• Number of boils cluster together = “Carbuncle” (aka Abscess)
- Clinical Features:
• Tender, red nodule which enlarges & may later discharge pus
• Painful
• Cellulitis may occur
• Fever/illness is possible
- Management:
o Treated aggressively with antibiotics and drainage

Public Domain: [Link]

El Pantera, CC BY-SA 3.0 <[Link] via Wikimedia Commons

FUNGAL INFECTIONS
FUNGAL INFECTIONS

FUNGAL INFECTIONS:
- Fungal Nail Infections (Dermatophytes, Candida Albicans, or Moulds)
- Superficial (skin, nails and hair):
- Dermatophytes (Tinea):
o Eg: Ringworm Fungi
§ 2 Common Genuses - (Tricophyton & Microsporum)
§ Infection Restricted to the Superficial Keratinised Layers of the skin
• Note: Keratin is the Fungi’s food source
§ Can Evoke Cellular immune responses
- Pathogenesis:
o Fungi ONLY Metabolizes Keratin:
§ :. Only infect the Stratum Corneum
§ Note: Can Also Invade Hair Shafts
- Presentation:
o Annular eruption with Irregular edge
o Central clearing Peripheral scaling
o Focal hair loss due to infection of Hair Follicle
o Focal pityriasis (Skin Flaking)
o Usually not pruritic
o “Tinea Versicolor” (Depigmentation of the Skin)
- Conditions Named Based On Location of Infection:
o Tinea Corporis (On Body)
o Tinea Capitis (On Head)
o Tinea Crura (Pubic Area)
- Diagnosis:
o Clinical Diagnosis
o Woods lamp – only Microsporum canis fluoresces
o Microscopy of hairs/nail shavings/skin shavings
- Treatment:
o Topical Antifungals:
§ Clotrimazole
§ Miconazole
o Oral Antifungals:
§ Fluconazole

Sarahrosenau on [Link], CC BY-SA 2.0 <[Link] via Wikimedia

Commons
PARASITIC INFECTIONS
PARASITIC INFECTIONS

SCABIES
- Organism:
o Sarcoptes scabii (Scabies Mite)
- Epidemiology:
o Human infestations originating from pigs, horses and dogs are mild and self-limiting
o Scabies infestations from other humans never cure without intervention
- Ecology:
o Mites live in stratum corneum (Don’t get any deeper)
o Eat stratum corneal Keratinocytes
o Make “tunnels” by eating
o Mating occurs on the hosts skin
o Fertilized Female Mites Burrow into the Stratum Corneum (1 mm deep)
o Salivary Secretions contain Proteolytic Enzymes →Digest Keratinocytes
- Transmission:
o High prevalence in children (50%) and adults (25%) in tropical remote communities
o Spread by close physical contact
- Presentation:
o Itch (Exacerbated at night and after hot showers)
o Itchy, Excoriated Rash on Trunk, associated with Scaly Burrows on the fingers and wrists
o Often vesicles and pustules on the palms and soles and sometimes on the scalp
- Diagnosis:
o Clinical Diagnosis:
§ Chronic itch with Symmetrical Rash
§ Burrows
o Skin Scraping - Look for Scabies Mites:
§ Intact larvae, nymphs or adults
§ Unhatched or hatched eggs
§ Moulted skins of mites
§ Fragments of moulted skins
§ Mite faeces
- Treatment:
o Topical Permethrin
o Or Oral Ivermectin (But not on PBS – Very Expensive)
o Environmental Measures:
§ Mites can contaminate bedding, chairs, floors, and even walls
• (Usually only a problem with crusted scabies)
§ Wash, sun, vacuum, surface insecticide
o Community Prevention:
§ Treat all close contacts – Especially in Indigenous Communities
§ Simultaneous Effective Treatment
o TREAT AGAIN IN 7 DAYS
Gzzz, CC BY-SA 4.0 <[Link] via Wikimedia Commons

Penarc, CC BY 3.0 <[Link] via Wikimedia Commons

Joel Mills, CC BY-SA 3.0 <[Link] via Wikimedia Commons

LICE (PEDICULOSIS)
- 3 Types:
o 1) Head Lice: Pediculus Humanus Capitis
§ Epidemiology:
• Common in Primary School Children in the Tropics
• Higher prevalence in Aboriginal Children
§ Diagnosis:
• Conditioner + Fine-Tooth Come
• Wipe combings on white tissue paper
o 2) Body Lice: Pediculus Humanus Corporis
§ Live on clothes, and come to the body to feed
o 3) Pubic Lice: Phthirus Pubis
§ Largely sexually transmitted
§ Blood Feeder
§ Can infect any Body Hair (Pubic/Trunk/Legs/Axilla/Beard) but rarely head
- Lifecycle:
o Eggs laid in hair (knits)
o Larvae grow into adults
o Adults – blood sucking (live in hair)
- Transmission:
o head-head contact
- Presentation:
o Scalp and Neck can be Itchy
o Nits are noticeable on the hairs
- Diagnosis:
o Best Method = ‘Conditioner & Comb Technique’:
§ Very Practical for parents
§ Cost Effective
§ High Sensitivity
§ Conditioner ‘Stuns’ the lice by suffocating them → Prevents them from running away
- Management/Treatment:
o Conditioner & Nit Comb
o Physical Removal
o Cut Hair
o Topical Insecticidal Cream
o Good idea to wash pillows and hats though – Hot Wash
o (Treat all body hair – for Pubic lice)
o Reasons for Treatment Failure:
§ Inadequate application of the product
§ Lice are resistant to insecticide
§ Failure to retreat to kill nymphs emerged from eggs
§ Reinfection

Public domain, via Wikimedia Commons:

[Link]
[Link]
VIRAL INFECTIONS
VIRAL INFECTIONS

HERPES SIMPLEX
- What is it?
o Common Mucosal Viral Infection that presents with localised blistering
o Can reside in a latent state
- 2 Types:
o Type 1: Typically facial/oral infections (Cold sores/fever blisters)
§ Occur mainly in infants & young kids
o Type 2: Mainly Genital
§ Occur after puberty (often transmitted sexually)
- Presentation:
o Stages of Infection:
§ 1) Prodromal Stage Vesicle or "blister" stage
§ 2) Ulcer stage
§ 3) Crust stage
o The virus grows down the nerves and out into the skin → Localised Blistering
o Neuralgia
o Lymphadenopathy
o High Fever
- Recurrences can be triggered by:
o Minor trauma/Other infections/UV radiation/Hormonal factors/Emotional
stress/Operations/procedures on face
- Treatment:
o Mild cases require no treatment
o Sun protection to prevent
o Oral Antiviral Drugs (Stop the virus multiplying)
- Complications:
o Encephalopathy
o Trigeminal Neuralgia (Neurogenic Pain)

Public Domain: CDC

CHICKEN POX (VARICELLA ZOSTER):
- What is it?
o Highly contagious disease
o Typically childhood disease (before 10yrs)
o One infection thought to confer lifelong immunity
- Organism:
o Varicella zoster virus (HHV3) (AKA: Chicken Pox Virus, Varicella, Zoster)
- Transmission:
o Highly Infectious
o From person to person
o Aerosol Droplets
o Direct contact with fluid from open sore
- Pathophysiology:
o Incubation Period ≈ 2wks
o (Chicken Pox) Initial Mucosal Infection → Viremia → Epidermal Lesions
§ May lead to → Latent infection of Dorsal Ganglion Cells of Sensory Nerves
o (Shingles) Reactivation of latent Varicella Zoster Virus in Peripheral Nerves
- Signs/symptoms:
o Itchy rash or red papules
o Begins on the Trunk →Face and Extremities
o May cover entire body
o High fever/headache/cold-like symptoms/vomiting/diarrhoea
- Diagnosis:
o Clinical Diagnosis
o Immunofluorescence
o Test for Elevated VZV-Specific Antibodies
§ (IgM – Primary Infection; IgG – Second Infection)
- Treatment:
o Symptomatic
o Resolves on its own
- Complications:
o Varicella During Pregnancy can → Congenital Varicella Syndrome:
§ Spontaneous Abortion (3-8% in 1st Trimester) or IUGR
§ Skin: Cutaneous Defects, Hypopigmentation
§ Neuro: Intrauterine Encephalitis, Brain Damage, Seizures, Developmental Delay
§ Eye: Chorioretinitis, Cataracts, Anisocoria
§ MSK: Limb Hypoplasia
§ Systemic: cerebral cortical atrophy
§ Renal: Hydronephrosis, Hydroureter
§ GI: GORD
§ CVS: Congenital Heart Defects
o Perinatal Varicella Infection:
§ severe → mortality rate of 30%
Camiloaranzales, Public domain, via Wikimedia Commons

F malan, CC BY-SA 3.0 <[Link] via Wikimedia Commons

HERPES ZOSTER (SHINGLES)
- What is it?
o Reactivation of Latent Herpes Varicella Zoster Virus
- Pathophysiology:
o Incubation Period ≈ 2wks
o (Shingles) Reactivation of latent Varicella Zoster Virus in Peripheral Nerves
- Presentation:
o Painful blistering rash along 1/more Dermatomes
o Virus is seeded to nerve cells in spinal cord
o Fever, malaise and headache
o Lymph nodes draining affected area are often enlarged/tender
o Can also result in nerve palsy
- Diagnosis:
o Clinical Diagnosis
o Test for Elevated VZV-Specific Antibodies
o PCR
- Transmission:
o Shingles are infectious
o From person to person
o Direct contact with fluid from open sore
- Treatment:
o Antiviral treatment
o Rest & analgesia
o Oral Antiviral

Gzzz, CC BY-SA 4.0 <[Link] via Wikimedia Commons

HPV WARTS (VERRUCA VULGARIS)
- What are They?
o = Benign Tumours of the skin
o Common in children
o Infectious – (Spread by direct contact)
- Organism:
o Typically from HPV (human papilloma viruses)
o HPV 6 & 11 → Genital & Cutaneous Warts
o HPV 16 & 18 → Cervical & Penile Ca
- Pathogenesis:
o HPV → Cellular Mutation → Hyper/Neo-Plasia
o → Wart Formation (Mostly Benign)
- Morphology:
o Gross:
§ Verrucous Warts
§ Intradermal Hard Cysts
o Microscopic:
§ Inward Growth Deep into the Skin
§ Koilocytic Keratinocytes (Dysplastic Squamous cells)
§ Central Blood Vessels
- Presentation:
o Common on back of fingers, toes and knees
o Common Warts (Skin/Plantar/Palmar)
o Genital Warts (Cervix, Vulva, Penis)
§ Note: Cervical Papillomas → Can cause cervical cancer
o Laryngeal Papilloma
- No Reliable Treatment:
o 50% of childhood warts disappear within 6mths; 90% are gone in 2 years
o Many don’t bother with treatment
o Surgical Excision/Chemical Treatment/Cryotherapy/Electrosurgery (Cauterise)
- Clinical Features:
o Contagious
o Central blood vessels → Bleed profusely when the surface is broken

Klaus D. Peter, Wiehl, Germany, CC BY 3.0 DE <[Link] via

Wikimedia Commons
PREMALIGNANT & MALIGNANT SKIN CONDITIONS
PREMALIGNANT & MALIGNANT SKIN CONDITIONS

ACTINIC KERATOSIS (SOLAR KERATOSIS)

- Aetiology:
• Sun Damage
- Pathogenesis:
• = Damage to the skin from UV (wrinkling, pigmentary change, actinic keratoses and cancer)
• Sun Damage due to Chronic Exposure to UV Radiation
- Morphology:
• Gross:
- Red/Tan, Irregular, Scaly Plaques
- Hyperkeratosis
- Inflammation/Ulceration/Crusting
• Microscopic:
- Dysplasia (Pre-Cancerous) & Atrophy
- Inflammation
- Hyperkeratosis AND Parakeratosis
- Loss of Papillary Dermis & Rete Ridges
- Atrophy of the Epithelium
- Very Large & Irregular Nuclei of Epidermal Cells
- Thick & irregular collagen bundles

Unattributable
- Clinical Features:
• The earliest sign = Freckling
• A Pre-Cancerous Skin-Growth
• They are most common on the face, back of the hands and forearms
• Solar keratoses are NOT cancer, however they are a sign of significant sun damage and are
therefore an indicator of higher risk for non-melanoma and melanoma skin cancer
- Management:
• Cryotherapy
• Shave/curettage/electrocautery
• Excision
• Imiquimod cream
James Heilman, MD, CC BY-SA 4.0 <[Link] via Wikimedia Commons
BASAL CELL CARCINOMA
- Aetiology:
• Sun Exposure
- Pathogenesis:
• Dysplasia & Tumorigenesis of Basal Epithelial Cells
• Slow Growing
• Rarely Metastasises (Locally Infiltrative, but don’t often Metastasise)
- Morphology:
• Superficial BCC’s
- Flat Red/Pink Shiny Macules or patches
- Indistinct Borders
• Nodular BCC's
- Pearly/red/translucent Nodules
• Other Gross Features:
- Blood Vessels
- Pearly/Shiny crust over the lesion
- Overlying telangiectasia
- Large Tumours may Ulcerate
• Microscopy:
- Clusters of blue Proliferating Basal Cells
- Burrows Deep into the Dermis
- Basal cells are pleomorphic
- “Palisading” appearance around the edge of the clusters of Basal cells (like the walls of a
palace)

John Hendrix, Public domain, via Wikimedia Commons

Klaus D. Peter, Wiehl, Germany, CC BY 3.0 DE <[Link] via

Wikimedia Commons
SQUAMOUS CELL CARCINOMA
- Aetiology:
• Chronic Sun Damage
• Industrial Carcinogens
• Tobacco
- Pathogenesis:
• Dysplasia & Tumorigenesis of Squamous Epithelial Cells
• Squamous Cell Mutation → Dysplasia → Neoplasia
- Morphology:
• Gross:
- Typically Tender Papules/Nodules with ROUGH, ADHERENT SCALE
- Hyperkeratosis
- Sometimes Erythematous base
- Often Ulcerate Centrally
- Often Present as Ulcers on Lips/Mucosa
• Microscopy:
- Dyskeratosis (↑Keratin production by Pleomorphic Squamous Cells)
1. ***Presence of Keratin “Pearls”
2. Pink on microscopy due to lots of keratin
- Whorls & Nests (Clusters) of malignant cells
- Clinical Features:
• 2nd commonest skin cancer after BCC
• They frequently grow rapidly and may be painful
• Malignant (Early Treatment via Wide Excision is Essential)
- Treatment:
• Wide excision
• Cryotherapy
• Adjuvant Radiotherapy

Source: Unattributable

Credit: [Link]
KERATOACANTHOMA
- Aetiology:
• Sun damage
- Epidemiology:
• Elderly / chronic sun-exposure / outdoor workers
• Fair skin
- Pathophysiology:
• Tumorigenesis of hair follicle skin cells
- Clinical Features:
• Erupting skin lesion
• Hard keratin core
• Irritating
- Management:
• Treated surgically → Excision → Pathology
• Cryotherapy (if <0.5cm)

Image Credit: Peter Mullineux / Shutterstock

MALIGNANT MELANOMA
- Aetiology:
• Sun Damage
• Congenital
• incidence is higher in the elderly
• 3rd Most Common Cancer in Both Men & Women
- Risk Factors:
• Family history
• Fair complexion
• Freckles
• Tendency to burn (Fitzpatrick type I/II skin)
• Severe Childhood Sunburn (Solar Skin Damage)
• Immunosuppression
• High number of common acquired naevi
• Large (>10cm) Congenital Naevi
• Dysplastic Nevus Syndrome (5 or more dysplastic naevi)
- Pathogenesis:
• Tumorigenesis of Melanocytes
• Most develop in an existing Naevus
• Superficial Spreading melanomas grow Laterally Initially, then begin to grow downwards
• Begin with a Radial Growth Phase (RGP)
- Grow wider (↑Diameter)
• Vertical growth Phase Melanoma (VGP)
- VGP will eventually supervene within most RGP melanomas and typically presents as a raised
area that is progressively growing
- Types of Melanoma:
• “Superficial Spreading Malignant Melanomas” - linked to intermittent intense sun exposure
(sunburns)
- Presents with a flat, usually pigmented, asymmetric macule that is changing is size, shape or
colour
- Slow Growing

[Link]

• “Lentigo maligna melanoma” – linked to high doses of cumulative sun exposure

- presents as an unevenly pigmented, asymmetric facial freckle that is changing in size, shape
or colour

[Link]
• “Nodular Melanoma” – Due to Medium Sun Exposure
- Tends to grow more rapidly in depth than other melanomas
- The majority of deeply invasive, High-risk Melanomas

[Link]

• “Acral Lentiginous Melanoma” – NOT due to sun exposure

- Affects soles of the feet, palms of the hands, toes, and fingers, and occurs in the nail
apparatus

[Link]

• “Amelanotic Melanoma”- Red Patches on the Skin

- Many melanomas are partially non-pigmented and up to 20% are almost completely without
pigmentation. Amelanotic melanomas generally present as a red, changing lesion though
they can be skin coloured

[Link]
- Morphology:
• Gross:
- Grow & Change Colour
- Maculo-Papular Lesion
- Irregular Shape, Colour & Depth – Distinguishing Features
- Pigmented
• Microscopic:
- Diagnostic Feature: Atypical (Dysplastic) Melanocytes ABOVE The Epidermis
- (Also Invade down into the Dermis)
- Nests/Clusters of Atypical Melanocytes
- Inflammatory Cells
- Mitotic Figures (Due to High Replication Rates)
- Clinical Features:
• Malignant
• Metastasize
- Prognostic Factor:
• Breslow Thickness
• Clark Levels
• TNM Staging:
- T = Size/Depth
- N = Nodal Involvement
- M = Distant Metastasis?
- Diagnosis:
• Dermoscopy is ESSENTIAL!!
• Skin exam without dermoscopy will only pick 60% of melanomas
• ABCD’s of melanoma:
- A – Asymmetry of Shape and Structure
1. Ie: One half doesn't match the other half (border/colour/structure within the lesion)
- B – Border Irregularity: The edges are ragged, blotched, or blurred
- C – Colour Variability: The pigmentation is not uniform. Shades of tan, brown, and black
may be present and red, white, grey and blue may add to the mottled appearance
- D – Diameter Increasing: A width >6mm (about the size of a pencil eraser)
1. Note: Any growth of a mole should be of concern
- E–
1. Evolving - any lesion that is changing or enlarging
2. Elevated - Different elevations/contours OR ANY change from ﬂat to elevated is of
concern
- F – Firm: A lesion that is ﬁrm, and also ones that are friable (easily damaged) are more likely
to be malignant. Whilst benign moles are raised, soft and “wobble” like jelly with pressure
- G – Growing: Signs of growth (Slow/Rapid) should raise concern
Scientific Figure on ResearchGate. Available from: [Link]
comparison-between-benign-and-malignant-skin-lesion-using-the-ABCD-rule_fig1_338262001

o 3 Point Checklist (>2 = Malignant):

§ (A Screening tool for Malignancy)
§ High Sensitivity, But Low Specificity (Many benign lesions score higher than 1)
§ 1) Asymmetry of Colour and /or Structure
• Judge by symmetry of Structure/Pattern, not outline
§ 2) Atypical Pigment Network:
• Note: Typical Pigment Network Grids correspond to Rete Ridges in the Dermis

• Atypical Networks = Lines are of different thickness & sizes of ‘holes’ are varied

§ 3) Blue-White Structures:
• Any White and/or Blue colour present in the lesions
• Include:
o ‘Peppering’ (Melanophages)
o Blue-white Veil (Orthokeratotic Hyperkeratosis overlying the Pigmented
Tumour)
o Whitish Scar (Fibrosis)

- Treatment:
• Early Detection & Removal = The Only Reliable Curative Treatment
• Follow-up = Those who have had a melanoma, have a 13% risk of another
- Prognostic Factor:
• Breslow Thickness:
- Tumour thickness measured from the granular layer of the epidermis to the deepest
identified tumour cell
- Best Available predictor of Prognosis
• Poor Prognostic Factors:
- Ulceration
- High Mitotic Rate
- Signs of Regression = Bad
• Clark Levels:
- Relateds to the Deepest invasive tumour cells
- Levels 1 – 5
- (Not the same as TNM Staging)
• TNM Staging:
- T = Size/Depth
- N = Nodal Involvement
- M = Distant Metastasis?

[Link]
Note: Just realise that despite subtle changes in appearance, the actual size and infiltration of the Melanoma can be
quite significant.
PEDIATRIC EXANTHEMS
PEDIATRIC EXANTHEMS

MEASLES VIRUS:
• Organism:
– Morbillivirus
• Transmission:
– Respiratory Route (Aerosol)
– Contact with fluids from infected person’s nose/mouth
• Pathogenesis:
– Typically a Respiratory Infection
– →Produces a Viremia → Rash
• Presentation:
– Fever
– URTI - Cough, Rhinorrhoea, Red Eyes
– Maculopapular Erythematous (Morbilliform) Rash
– “Koplik’s Spots” – Seen on the Inside of the Mouth
• Complications Include:
– Croup
– Otitis Media
– Enteritis with diarrhoea
– Febrile convulsions
– Encephalitis (Serious)
– Subacute Sclerosing Panencephalitis (very rare)
§ (Chronic, progressive Encephalitis caused by persistent infection with immune-resistant
Measles Virus)
§ No Cure
§ Fatal
• Diagnosis:
– Clinical Diagnosis (Generalised Maculopapular Rash + Fever)
– Presence of Measles IgM Antibodies
– PCR of Respiratory Specimens
• Treatment:
– No Specific Treatment
– Prevented by MMR Vaccine
• Prevention:
– Attenuated MMR Vaccine (Admin at 12mths & 4yrs)
– Developing Countries: Low Herd Immunity → Higher Prevalence
§ Relatively High Death-Rates in Non-Immune

Photo Credit:Content Providers(s): CDC/Dr. Heinz F. Eichenwald, Public domain, via Wikimedia Commons
CDC, Public domain, via Wikimedia Commons

Public domain: CDC

RUBELLA VIRUS (“GERMAN MEASLES):
• Organism:
o Rubella Virus
• Transmission:
o Respiratory Route
o (Human Reservoir Only)
• Presentation:
o Initial Flu-Like Symptoms
o * Rash on Face → Spreads to Trunk & Limbs
§ Pink-Red, Itchy
o Low-grade Fever, Lymphadenopathy, Joint Pains, Headache, Conjunctivitis
• Prognosis:
o Typically Benign
o Typically Lasts 1-3 Days (Children Recover Quicker)
o Complications may include arthritis, thrombocytopenia purpura, and encephalitis
o *HOWEVER, Maternal Infection During PREGNANCY can be SERIOUS!!
§ If Infected in the 1st 20wks of Pregnancy → Congenital Rubella Syndrome
• →Abortion
• →Cardiac/Cerebral/Ophthalmic/Auditory Defects
§ Specific Foetal Damage Depends on Organ Development @ the Time:
• The 1st Trimester is Worst, as Organ Development occurs during this time
• After 1st Trimester, Organ Growth is the main process
• Diagnosis:
o Clinical Diagnosis
o Presence of Virus-Specific IgM Antibodies
• Treatment:
o No Specific Treatment
o Controlled in Australia by vaccination (MMR Vaccine)
o Test pregnant women for immunity early
• Prevention:
o (Note: Rubella Itself is relatively Benign, so why bother Vaccinating?)
o MMR Vaccine:
§ (Live Attenuated)
§ #1 Aim: Prevent Rubella in Pregnant Women → ↓Congenital Rubella Syndrome
§ Aimed at BOTH Males & Females to ↓Male Transmission to Pregnant Females

[Link], CC BY-SA 4.0 <[Link] via Wikimedia Commons

[Link]

[Link]
HUMAN PARVOVIRUS B19 (“5TH DISEASE”)
• Organism:
o Parvovirus B19
• Transmission:
o Respiratory Droplet
o Blood-Borne
• Pathophysiology:
o Virus Replicates in Rapidly-Dividing Cells (Eg: Bone Marrow RBC Precursors)
§ → RBC Haemolysis
§ → Severe Anaemia
§ → Can Result in Haemolytic Crisis
o The receptor for the virus is a globoside, which is abundant on tissues of mesodermal origin
o Can cross the placenta into the foetus
§ → Foetal Anaemia
• Presentation:
o Fever/Malaise
o Characteristic Rash
§ Teenagers: ‘Papular Purpuric Gloves & Socks Syndrome’
§ Children: ‘Slapped Cheek Syndrome’
• Note: Foetal Infection →Foetal Damage or Abortion

Andrew Kerr, Public domain, via Wikimedia Commons

Sandyjameslord, CC BY-SA 4.0 <[Link] via Wikimedia Commons
SCARLET FEVER:
- Organism:
o Certain strains of Strep pyogenes (Which carry a Bacteriophage – A virus infecting the bacteria →
Produce an Eruthrogenic toxin)
- Epidemiology:
o Mostly occurs in kids aged 4-8yrs
- Pathogenesis:
o GAS infection of Tonsils/Pharynx/Skin
o Exotoxin Released by Strep-Pyogenes → Local effect on Tonsils/Pharynx/Skin
o →Abnormalities of tongue
§ Initially covered with white exudate
§ Exudate is shed
§ inflammation of underlying tissue
o → Diffuse, Erythematous Exanthem
- Treatment:
o Antibiotics (Usually penicillin for 10days; or single IM dose; or erythromycin if penicillin allergic)
o Antipyretics
o Fluids
o Oral antihistamines to relieve the rash
- Longer-Term Complications:
o Rheumatic fever
o Glomerulonephritis

1 - Estreya at English Wikipedia., CC BY 2.5 <[Link] via Wikimedia Commons

2 - [Link], CC BY-SA 3.0 <[Link] via Wikimedia
Commons

Afag Azizova, CC BY-SA 3.0 <[Link] via Wikimedia Commons

SCALDED SKIN SYNDROME (SSS):
• Organism:
o Staph-Aureus →Releases two Exotoxins (epidermolytic toxins A and B) from toxigenic strains
• Pathogenesis:
o Toxins Degrade Desmosomes → Acantholysis
• Presentation:
o Fever, Irritability, Rash
o 24-48hrs later → Widespread Red Blistering Skin that looks like a burn or scald
o occurs mostly in children younger than 5 years, particularly neonates
• Diagnosis:
o Tzanck smear
o Skin biopsy
• Treatment:
o IV Antibiotics to eradicate staph infection (Eg: Flucloxacillin/Cephalosporin/clindamycin)
o Vancomycin if MRSA suspected

Creative Commons Attribution 4.0 International License;

[Link]

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

TOXIC SHOCK SYNDROME (TSS):
• Organism:
o TSST-1-producing Staphylococcus aureus
o or TSST-1-producing Strep-pyogenes
• Pathogenesis:
o Gram Positive Organisms release Exotoxins (Superantigens)
o → Mass, Non-Specific activation of T-Cells → Overproduction of Cytokines → Systemic Vasodilation
→ Shock
o Cutaneous Response to toxins = Sunburn-like Rash + Desquamation
• Presentation:
o Rapid Onset Fever
o Generalised Skin/Mucosal Erythema
o Shock → Hypotension & Multi-System Failure
o Shedding of skin in large sheets (especially palms and soles) 1-2wks after onset of illness
• Treatment:
o Prompt treatment is required to avoid failure of vital organs (Eg: Liver, lungs & heart)
o Remove source of infection
o IV Antibiotics (Flucloxacillin/cephalosporin/vancomycin)
o IV Fluids & supportive management
o Dialysis may be needed

N Engl J Med 2013; 369:852; DOI: 10.1056/NEJMicm1213758

PROCEDURAL DERMATOLOGY
PROCEDURAL DERMATOLOGY

Local Anaesthetic:
- Mechanism of Action:
o Use-Dependent blockade of Voltage-Gated Sodium Channels on Nerves
§ → Prevents Action Potential Conduction along Sensory Nerves
o Note: Very Quick Onset of Action
o Note: Also causes vasodilation → Short Duration of Action (If without adrenaline)
- Lignocaine – Most Common:
o Rapid Onset (1-5mins)
o Medium (30-120mins)
o Max Dose: 4mg/kg
§ ≈ 50mL @ 1% Lignocaine
o (Note: 1% Lignocaine = 1g/1000mL)
- + Adrenaline:
o → Improves Haemostasis
§ → ↓Bleeding
o → ↓Systemic Absorption
§ → ↓Risk of systemic toxicity
§ → Prolonged Effect
o Max Dose: 7mg/kg (Higher Dose than without adrenaline)
o Note: DO NOT USE IN DIGITS OR PENIS (Or anywhere else with “End Arteries”)
o Note: DO NOT USE in LONG QT-Syndrome
- Naropin (Ropivicaine):
o Longer onset of action
o Longer acting than lignocaine
o Max Dose: 2-3mg/kg
- Topical Anaesthetic:
o Xylocaine Gel - Useful for Mucosal Surfaces (Eg: Oral Mucosa)
o ELMA Cream – Useful for topical anaesthesia of skin
- Nerve Blocks:
o Digital Block (Ring Block)
§ (Most Common)
§ Blocks Digital Nerves
§ Use 2% Lignocaine (Because you want to inject as little as possible)
o Wrist Blocks:
§ Blocks Radial, Median, & Ulnar Nerves
§ → Totally anaesthetizes the hand

Curettage & Electrocautery:

- Indications:
o Warts
o Keratoses
o Molluscum contagiosum
o Curettes can also be used for curette biopsy
- Wound Healing
o The curette wound can take some time to heal
o If it is just a light curette such as tiny seborrheic keratoses with no cautery they can heal in a few
days
o A full curettage and electrodessication on the trunk might take 4 to 6 weeks to heal
Cryotherapy:
- Cryotherapy is a very useful form of treatment for a number of benign skin lesions and few pre-malignant
and malignant skin lesions
- Liquid Nitrogen = The gold standard
- Indications:
o Benign lesions:
§ Molluscum contagiosum
§ Seborrheic keratosis
§ Skin tags
§ Warts
o Premalignant lesions:
§ Actinic keratoses
§ Actinic Chelitis
o Malignant lesions:
§ Superficial BCC
- Effects of Cryotherapy – 3 Main Groups:
o 1) Those responses we expect to happen:
§ Pain on treatment and for a period afterwards
§ Oedema and swelling of the treated site and the surrounding tissue (Eg: periorbital swelling
after treatment of lesions on the forehead)
§ Vesicle and bulla formation
§ Exudation weeping and crust formation
o 2) Temporary Adverse Outcomes:
§ Hypopigmentation
§ Hyperpigmentation
§ Secondary Infection
o 3) Permanent Adverse Outcomes:
§ Permanent Hypopigmentation
§ Scarring + Possible Retraction
§ Allopecia
§ Nail Dystrophy

Biopsy Techniques:
- Many different Techniques
- Technique depends on the Nature of the Lesion & Information Required
- Types:
o Punch biopsy
§ Leaves Minimal Scarring
§ Best for Cosmetically Sensitive Areas – (Eg: Face)
o Shave Biopsy
§ Fast and easy to perform
§ Requires little equipment
§ A shave biopsy is excellent for nodular bulky lesions which are easy to shave off for histology
o Curette biopsy
§ Fast and easy to perform
§ Requires little equipment
§ A shave biopsy is excellent for nodular bulky lesions which are easy to shave off for histology
o Incision Biopsy
§ A biopsy set is required with scalpel, forceps, needle holders and fine scissors as well as a
suture to perform a small incisional ellipse. Be sure to go through the dermis to get a full
thickness specimen
§ Advantages:
§ Provides the best specimen for the pathologist to assess the tissue adequately
o Excision biopsy
§ Similar to an incisional biopsy but the whole lesion is excised
§ Good pathology specimen
Wound Design:
- Wounds should be designed so that scars sit in or parallel with the relaxed skin tension lines or the cosmetic
junction lines
- Excision margins are important to ensure complete removal of the lesion. For benign lesions the margins are
usually 2mm to 5 mm. For malignant lesions the margins can vary from 3mm up to 2 cm depending on the
nature of the pathology

Surgical Wound Repair:

- Suture Materials:
o Synthetic Non-Absorbable:
§ Nylon
§ Polypropylene
§ (Used on external surfaces where they are easily removed)
o Synthetic Absorbable:
§ Monocryl
§ Vicryl (Polylactin)
§ (Broken down by the body via Hydrolysis &/or Proteolytic Enzymatic Degradation)
o Non-Synthetic Non-Absorbable:
§ Silk
o Non-Synthetic Absorbable:
§ Catgut (Being Phased out)
- Suture Sizes:
o Scale from 1-6 (1 = Thinnest (0.4mm); 2 = Thickest (0.8mm)
- Surgical Wound Repair:
o Primary Repair:
§ 6-8hrs
o Delayed Primary Repair
§ In 72hrs
§ In surgical conditions
o Secondary Repair:
§ After 72hrs
§ In surgical conditions
- Important Pre-Requisites:
o Wound needs to be CLEAN!
§ Eliminate Dead Tissue/Dead Space/Haematoma/Foreign Bodies
o Finest Suture Material
o Minimise Tension
o Suture Removal @ Appropriate time for site of injury
§ 1-2 wks
Skin Grafts Vs Skin Flaps:
- Skin Grafts:
o Has been totally dethatched from its original location
o :. Has NO intrinsic Blood Supply
§ :. Must be grafted onto Vascularised Tissue
§ It will initially survive via Simple Diffusion of Nutrients
§ Eventually, Neovascularisation → New Blood Supply
o Types:
§ Full Thickness Graft (FTG)
• All of the Dermis & Epidermis
§ or Split Skin Graft (SSG)
• All of the Epidermis & some of the Superficial Dermis

Unattributable
- Skin Flaps:
o Has NOT been detached from its original location
o :. Still Has Intrinsic Blood Supply
o Indications:
§ Poor Vascularity of Location (Eg: Bare bone, Bare tendons)
§ Vital Structures (Eg: Exposed Vessels/joints)
§ Cosmetics (Eg: Face) – Usually gives a better result than a skin graft
o 3 Basic Types:
§ Rotation
§ Advancement
§ Transposition
- “Free” Flaps:
o = Basically a Skin Graft, but the Blood Supply is Reconstituted using Microsurgery to reconnect the
Artery and Vein

Unattributable
SKIN PATHOLOGY – UNDER A MICROSCOPE
SKIN PATHOLOGY – UNDER A MICROSCOPE

Common Histopathological Terms:

• Hyperkeratosis:
o Hyperplasia of the Stratum Corneum
o Note: Also Thickening of the Dermis & Rete ridges
o Clinical appearance = scaling
§ Psoriasis, eczema

• Parakeratosis:
o A Pattern of Keratinization Characterized by Retention of Nuclei in the stratum corneum (due to very
very rapid keratinisation –no chance to mature & lose the nucleus)
§ (Note: This is normal on mucous membranes)
o Seen in many cases of hyperkeratosis
o Clinical appearance = Scaling
• Papillomatosis:
o Hyperplasia of the Papillary Dermis
o (The whole skin becomes folded – Papillary Projections – Typical in infections)
o Caused by Neoplastic-verrucous ca, venous stasis, viral

• Dyskeratosis:
o Abnormal Keratinization due to Carcinoma
§ Very typical of malignancy
o Cells containing high amounts of keratin beneath the Stratum Corneum
§ → Keratin Cysts
o Note: Also many inflammatory cells
• Acanthosis:
o Epidermal Hyperplasia (Increased number of epidermal cells, deepening of rete ridges) → Thickening
of the Epidermis
o Seen in: Eczema, psoriasis

o Types of Acanthosis:
§ Psoriasiform (Regular) Acanthosis
§ Irregular Acanthosis
§ Papillated Acanthosis (Epidermal Growth goes above the normal level)
§ Pseudoepitheliomatous/pseudocarcinomatous (Epidermal Growth Infiltrates into the
dermis)
• Acantholysis:
o Loss of Intercellular Connections
§ Antibody-Mediated Destruction Against Desmosomes
§ → “Breaking down of brick wall” → Blisters
o Seen in: Pemphigus (a group of Blistering Autoimmune Diseases)

• Spongiosis:
o Inflammation and Intercellular Epidermal Oedema
o →Separation of cells without breakdown of cell-junctions (Not like Acantholysis)
o Aetiology: The initial response to any damage to the epidermis (scratching/irritants/Etc )
o Seen in: Eczema, Pemphigus, Seborrheic dermatitis
EXAMPLES OF EXAM QUESTIONS:
EXAMPLES OF EXAM QUESTIONS:

1. Lesions following viral fever & sore throat. Lesions have a central clearing (Target-eyed Lesions), are red.
Diagnosis?
a. Erythema Multiforme
2. Itchy, lesion on wrist for 3 days following wearing new bracelet. Microscopy shows spongiosis
(intraepidermal oedema) Diagnosis?
a. Acute Eczema/Contact Dermatitis (Due to allergy against material in bracelet)
b. (Not Urticaria – would present within hours, and doesn’t have spongiosis)
3. 84yr old, scalp lesions. (It is Actinic Keratosis) What is the diagnostic feature you would see under the
microscope?
a. Solar Elastosis (Very specific to solar damage)
b. Also have Parakeratosis (but is also seen in other conditions)
4. 41 yr old male, generalised very itchy rash, swollen lips. Diagnosis?
a. Urticaria
5. What is the characteristic microscopic feature of Urticaria?
a. Dermal Oedema (As opposed to Spongiosis, which occurs after 3-4 days) due to mast cell
degranulation
6. Rash 6 days after giving blood @ the site of the Band-Aid. Diagnosis?
a. Contact Dermatitis
7. What is the microscopic characteristics of Acanthosis:
a. diffuse epidermal hyperplasia.[1] Acanthosis implies increased thickness of stratum spinosum
8. 82 yr male, lesions on hand and ear. Microscopy shows irregularity of cells, and the lesion is shiny,
erythromatous plaques. Diagnosis?
a. Squamous Cell carcinoma
9. 48yr female, large flaccid blisters. Some broken with crusting. Diagnosis?
a. Pemphigus (As opposed to Bullous Pemphigoid)
10. 28yr male, asymptomatic lesions for 3 weeks on chest & back. Diagnosis?
a. Tinea Versicolor
11. 81yr male, surfing enthusiast, lesions on cheek or 3 years. Slowly increasing. Diagnosis?
a. Actinic Keratosis (Sun damage)
12. 21yr male, lesions on face since 4 weeks. Slowly increasing. Itchy, but no pain. Diagnosis?
a. Impetigo (Staphylococcal)
13. 71yr female, recurrent flaccid blisters. Diagnosis?
a. Pemphigus Vulgaris
14. Asymptomatic mole. Growing. Diagnosis?
a. Melanoma
15. 3yrs lip licking → Crusting. Diagnosis?
a. Impetigo
16. 13 yr girl. Allopecia, Erythema. Diagnosis?
a. Tinea Capitis Infection
17. 83yr nodular lesion on face for 2 years. Diagnosis?
a. BCC
18. Recurrent small itchy vesicles. Lesions exacerbate following eating bread.
a. Dermatitis Herpetiformis
Case 1)

Clinical Description:
- Small, brown papule
- 9mm diameter
- Irregular shape
ABCD (EFG) Criteria:
- Asymmetrical
- Border Irregularity
- Colour Variability
- Diameter increasing unknown
- Don’t know if Evolving
- Elevated
Three Point Checklist Score (Malignant):
- Asymmetry?
o Yes
- Atypical Network?
o No
- Blue-white Structures?
o Yes
Provisional Diagnosis:
- Potentially malignant BCC
Management:
- Excision
Case 2)

Clinical Description:
- 5mm diameter
- Papular-Plaque
- Brown
- Well defined border
- Regular shape & Pigment distribution
- Has ridges & fissures/como-like openings
ABCD (EFG) Criteria:
- Symmetrical
- Regular borders
- Regular Colour
- Diameter not increasing
- Not evolving
- Elevated
- Not growing
Three Point Checklist Score:
- Asymmetry?
o No
- Atypical Network?
o No
- Blue-White Structures?
o No
Provisional Diagnosis:
- Benign Seborrheic Keratosis
Management:
- Monitor
- No management needed
Case 3)

Clinical Description:
- 1cm wide plaque
- Well defined border
- Regular shape
- Regular pigmentation
ABCD (EFG) Criteria:
- Symmetrical
- Well defined border
- Regular Colour
- No history of change (diameter/evolution)
Three Point Checklist Score:
- Asymmetry?
o No
- Atypical Network?
o No
- Blue-Grey Structures?
o Yes
Provisional Diagnosis:
- Benign
- Blue Naevus
Management:
- Monitor
- No Management Needed
Case 4)

Clinical Description:
- Small pigmented lesion
- Macule (not raised)
- Irregular border
ABCD (EFG) Criteria:
- Symmetrical pattern, asymmetrical shape
- Irregular Border
- Consistent Colour
- No history of increasing Diameter/Evolution
Three Point Checklist Score:
- Asymmetry?
o No
- Irregular Network?
o No
- Blue-Grey Structures?
o No
Provisional Diagnosis:
- Benign
- Ink-Spot Lentigo
Management:
- No management needed
Case 5)

Clinical Description:
- Scaly raised, erythematous Macule
- Poorly defined border
- Erythematous base
- scaling
ABCD (EFG) Criteria:
- Asymmetrical
- Irregular border
- Consistent Colour
- Increasing Diameter
- Evolving
Three Point Checklist Score:
- Asymmetry?
o Yes
- Irregular Network?
o No
- Blue-Grey Structures?
o Yes
Provisional Diagnosis:
- Malignant
- Amelanotic Melanomas
Management:
- Excision
Case 6)

Clinical Description:
- Large pigmented plaque
- Warty surface
- No history of change
- Well defined border
ABCD (EFG) Criteria:
- Symmetrical in shape but asymmetrical in structure
- Well defined Border
- Consistent Colour except for area of white regression
- Constant diameter
- No history of evolution
Three Point Checklist Score
- Asymmetry?
o No
- Irregular Network?
o No
- Blue-White Structures?
o Yes
Provisional Diagnosis:
- Benign
- Birth Mark (congenital Naevus)
Management:
- None needed
Case 7)

Clinical Description:
- Asymmetrical macula-papular lesion
- Crusted surface
- Large
- Pigmented
- Milia like cysts, comedo-like openings
ABCD (EFG) Criteria
- Asymmetrical
- Well-Defined Borders
- Regular Colour
- Diameter ≈ 1cm
Three Point Checklist Score
- Asymmetry?
o Yes
- Irregular Network?
o No
- Blue White Structures?
o Yes
Provisional Diagnosis:
- Seborrheic Keratosis
- Benign
Management
- None Needed
Case 8)

Clinical Description:
- Papular lesion on chest
- 7mm diameter
- Well defined borders
- Regular shape
- Increasing in size over 12 mths
ABCD (EFG) Criteria:
- Symmetry in shape, but Asymmetry in colour
Three Point Checklist Score:
- Asymmetry?
o Yes
- Irregular Network?
o No Network (Many melanomas don’t have network)
- Blue White Structures?
o Yes
Provisional Diagnosis:
- Malignant
- Invasive Melanoma
Management:
- Excision
Case 9)

Clinical Description:
- Pigmented macule
- Symmetrical
- Well defined, regular border
- Enlarging
- 1cm diameter
ABCD (EFG) Criteria:
- Symmetrical
- Regular, well defined borders
- Regular consistent colour
- Diameter 10mm
- Evolving? Growing
Three Point Checklist Score:
- Asymmetry?
o No
- Irregular network?
o No
- Blue-white structures?
o No
Provisional Diagnosis:
- Solar Lentigo
Management
- None Needed
Case 10)

Clinical Description:
- Pigmented Macule
- Irregular Colour & Border
- Asymmetrical
- Long-Standing
- Regression in the centre → white area
ABCD (EFG) Criteria:
- Asymmetrical
- Irregular Border
- Irregular Colour
- Diameter 9mm
- Evolving? NO
Three Point Checklist Score
- Asymmetrical?
o Yes
- Irregular Network?
o Yes
- Blue white structures?
o Yes
Provisional Diagnosis:
- Melanoma evolving inside a dysplastic naevi
Management:
- Excision
Case 11)

Clinical Description:
- Enlarging Macule
- Irregular Border
- Consistent Colour
- Symmetrical
- Faint Network
ABCD (EFG) Criteria:
- Symmetrical
- Irregular Borders
- Consistent Colour
- 1cm diameter
Three Point Checklist Score
- Asymmetrical?
o Yes
- Blue white Structures?
o No
- Irregular Pigment Network?
o No
Provisional Diagnosis
- Solar Lentigo
Management
- None
Case 12)

Clinical Description
- Pigmented papule
- Irregular Border
- Asymmetrical
- Irregular colour pattern
ABCD (EFG) Criteria
- Asymmetrical
- Irregular Border
- Irregular Colour
- Diameter – Not Growing
- Evolving? no
Three Point Checklist Score
- Asymmetrical
o Yes
- Blue white structures
o Yes
- Atypical Network
o yes
Provisional Diagnosis
- Melanoma
Management:
- Excision
Case 13)

Clinical Description:
- Telangiectasia
ABCD (EFG) Criteria:
- Asymmetrical
- Ill-defined border
- Irregular colours
- Diameter – 5mm
- Evolving - unknown
Three Point Checklist Score
- Asymmetrical:
o Yes
- Blue White Structures?
o Yes
- Irregular network?
o no
Provisional Diagnosis:
- BCC
Management
- Excision
Case 14)

Clinical Description
- Ugly duckling
- Poorly defined border
Three Point Checklist Score
- Irregular Network
o yes
Provisional Diagnosis
- Invasive Melanoma

Case 15)

Clinical Description:
- Diffuse,
- Asymmetrical
- Pigmented lesion
Three Point Checklist Score
- Asymmetrical
- Irregular network
- White structures
Provisional Diagnosis:
- Melanoma Insitu
Case 16)

Clinical Description:
- Glomerular Vessels
Three Point Checklist Score:
- Asymmetry
Provisional Diagnosis:
- Bowens Disease (Intraepidermal Carcinoma)

Case 17)

Three Point Checklist Score:

- Irregular network
- Asymmetrical
- Inverse pigment Network
Provisional Diagnosis:
- Melanoma
Management:
- Excision
Case 18)

Clinical Description
- Fine telangiectasia
Three Point Checklist Score
- Asymmetrical
- Blue white structures
Provisional Diagnosis:
- BCC

Case 19)

Three Point Checklist Score

- Asymmetrical
- Blue white structures
- Irregular Pigment Network
Provisional Diagnosis
- Melanoma
Management:
- Excision
Case 20)

Three Point Checklist Score:

- Asymmetrical
- White Structures
Provisional Diagnosis:
- Melanoma
Management
- Excision

Dermatology Notes for Medical Students
No ratings yet
Dermatology Notes for Medical Students
35 pages
Clinical Dermatology PDF
No ratings yet
Clinical Dermatology PDF
169 pages
Dermatology Notes for Med Students
No ratings yet
Dermatology Notes for Med Students
170 pages
Clinical Dermatology
No ratings yet
Clinical Dermatology
170 pages
Dermatology - 3rd Ed
100% (1)
Dermatology - 3rd Ed
137 pages
Keratinocytes: Skin's Protective Cells
No ratings yet
Keratinocytes: Skin's Protective Cells
16 pages
11.integumentary System
No ratings yet
11.integumentary System
76 pages
Skin Structure
No ratings yet
Skin Structure
14 pages
2 The Integumentary Real
No ratings yet
2 The Integumentary Real
137 pages
Integumentary System Overview: Skin Functions
No ratings yet
Integumentary System Overview: Skin Functions
29 pages
Anatomy and Functions of Human Skin
No ratings yet
Anatomy and Functions of Human Skin
5 pages
Derma Outline Complete
No ratings yet
Derma Outline Complete
51 pages
Andrews - Chapter 1 - Skin Basic Structure and Function
No ratings yet
Andrews - Chapter 1 - Skin Basic Structure and Function
38 pages
13.integumentary System
No ratings yet
13.integumentary System
54 pages
Integumentary System 2021
No ratings yet
Integumentary System 2021
53 pages
Integumentary System 1-1 PDF
100% (1)
Integumentary System 1-1 PDF
92 pages
Skin Structure and Function Overview
No ratings yet
Skin Structure and Function Overview
8 pages
Skin and Body Membranes Overview
No ratings yet
Skin and Body Membranes Overview
14 pages
Integumentary System Overview: Skin, Hair, Nails
No ratings yet
Integumentary System Overview: Skin, Hair, Nails
67 pages
Skin Anatomy
No ratings yet
Skin Anatomy
71 pages
Integumentary System - Uwi (Compatibility Mode)
No ratings yet
Integumentary System - Uwi (Compatibility Mode)
29 pages
Layers of The Skin
No ratings yet
Layers of The Skin
49 pages
Chapter 5
100% (1)
Chapter 5
14 pages
Superficial Bacterial Infections in Dermatology
No ratings yet
Superficial Bacterial Infections in Dermatology
35 pages
Skin Structure
No ratings yet
Skin Structure
45 pages
Microscopic Analysis of The Integumentary System
No ratings yet
Microscopic Analysis of The Integumentary System
9 pages
Overview of Skin Structure and Functions
No ratings yet
Overview of Skin Structure and Functions
17 pages
Histology of the Integumentary System
No ratings yet
Histology of the Integumentary System
80 pages
Anatomy and Functions of Skin Layers
No ratings yet
Anatomy and Functions of Skin Layers
51 pages
Integumentary System
No ratings yet
Integumentary System
54 pages
Integumentary System Overview and Functions
No ratings yet
Integumentary System Overview and Functions
97 pages
(Medicalstudyzone - Com) Elite Dermatology
100% (1)
(Medicalstudyzone - Com) Elite Dermatology
197 pages
Histology of Skin-20.5.22
No ratings yet
Histology of Skin-20.5.22
70 pages
Integumentary System Overview and Functions
100% (1)
Integumentary System Overview and Functions
67 pages
Understanding the Integumentary System
No ratings yet
Understanding the Integumentary System
19 pages
Overview of Integumentary System
No ratings yet
Overview of Integumentary System
109 pages
Overview of the Integumentary System
No ratings yet
Overview of the Integumentary System
55 pages
VIII. The Integumentary System.
No ratings yet
VIII. The Integumentary System.
11 pages
Dermatology Basics: Skin Structure & Function
No ratings yet
Dermatology Basics: Skin Structure & Function
23 pages
Dermatology Basics for Medical Students
No ratings yet
Dermatology Basics for Medical Students
12 pages
Intug System
No ratings yet
Intug System
42 pages
Skin Structure and Functions Overview
No ratings yet
Skin Structure and Functions Overview
40 pages
Introduction to Dermatology Basics
No ratings yet
Introduction to Dermatology Basics
102 pages
01 - Skin Structure and Function - DR Ayman Al-Wadei
No ratings yet
01 - Skin Structure and Function - DR Ayman Al-Wadei
88 pages
Epidermis: Cell Types and Functions
No ratings yet
Epidermis: Cell Types and Functions
16 pages
Skin Histology Overview and Functions
No ratings yet
Skin Histology Overview and Functions
48 pages
Online Practice Tests, Live Classes, Tutoring, Study Guides Q&A, Premium Content and More
No ratings yet
Online Practice Tests, Live Classes, Tutoring, Study Guides Q&A, Premium Content and More
43 pages
Overview of the Integumentary System
100% (1)
Overview of the Integumentary System
16 pages
0401 Histo Lecture
No ratings yet
0401 Histo Lecture
57 pages
Integumentary System Overview and Functions
No ratings yet
Integumentary System Overview and Functions
8 pages
Dermatology Atf
No ratings yet
Dermatology Atf
438 pages
Anatomy and Histology of Skin Overview
No ratings yet
Anatomy and Histology of Skin Overview
10 pages
Integumentary System Structure & Function
No ratings yet
Integumentary System Structure & Function
55 pages
Soft Tissue Reconstruction Overview
100% (2)
Soft Tissue Reconstruction Overview
201 pages
Overview of the Integumentary System
No ratings yet
Overview of the Integumentary System
8 pages
Asst. Professor Posting Application
No ratings yet
Asst. Professor Posting Application
7 pages
Engine Room Watchkeeping Guide
No ratings yet
Engine Room Watchkeeping Guide
1 page
Zero Consiousness Sutra
No ratings yet
Zero Consiousness Sutra
6 pages
Metal by Tutorials 2ed
100% (1)
Metal by Tutorials 2ed
722 pages
Water Management in Puntland
100% (1)
Water Management in Puntland
8 pages
Mercedes OM 460 LA Engine Overview
No ratings yet
Mercedes OM 460 LA Engine Overview
2 pages
Reading and Writing - 8th Grade
No ratings yet
Reading and Writing - 8th Grade
10 pages
Supplier List - Value First
No ratings yet
Supplier List - Value First
2 pages
Qutatation For Courier
No ratings yet
Qutatation For Courier
17 pages
Municipal Solid Waste Thesis Help Guide
100% (4)
Municipal Solid Waste Thesis Help Guide
5 pages
Understanding ICD-10-CM Conventions
No ratings yet
Understanding ICD-10-CM Conventions
9 pages
2009.Dehaan-essay-Teaching Creativity and Inventive Problem Solving in Science
No ratings yet
2009.Dehaan-essay-Teaching Creativity and Inventive Problem Solving in Science
10 pages
National Standards of Organic Farming
50% (2)
National Standards of Organic Farming
3 pages
Work, Power, and Energy Calculations
No ratings yet
Work, Power, and Energy Calculations
25 pages
Bhaskara II
No ratings yet
Bhaskara II
7 pages
Understanding Water Properties and Behavior
No ratings yet
Understanding Water Properties and Behavior
3 pages
Flexural Vibrations of Delaminated Beams
No ratings yet
Flexural Vibrations of Delaminated Beams
21 pages
Medical Combining Forms Guide
No ratings yet
Medical Combining Forms Guide
22 pages
Global Warming Eassy
No ratings yet
Global Warming Eassy
7 pages
USP-NF 71 Sterility Tests
No ratings yet
USP-NF 71 Sterility Tests
18 pages
SEW-EURODRIVE RF80A Parts List
No ratings yet
SEW-EURODRIVE RF80A Parts List
1 page
Momentum Transfer in Fluid Mechanics
No ratings yet
Momentum Transfer in Fluid Mechanics
6 pages
Empirical and Molecular Formula Guide
100% (1)
Empirical and Molecular Formula Guide
2 pages
7 2 Aldehydes and Ketones A Level Only HgQs8JCg9gzMPCmd
No ratings yet
7 2 Aldehydes and Ketones A Level Only HgQs8JCg9gzMPCmd
24 pages
Hotel California
No ratings yet
Hotel California
2 pages
In This Place Rulebook 1.0
No ratings yet
In This Place Rulebook 1.0
18 pages
JM Gas Processing Market Brochure c2018
No ratings yet
JM Gas Processing Market Brochure c2018
20 pages
Caterpillar CAT 416E BACKHOE LOADER (SHA00001-UP) Operation and Maintenance Manual Instant Download
No ratings yet
Caterpillar CAT 416E BACKHOE LOADER (SHA00001-UP) Operation and Maintenance Manual Instant Download
21 pages
Rotating Gate
100% (1)
Rotating Gate
34 pages

Lichen Simplex Chronicus Overview

Uploaded by

Lichen Simplex Chronicus Overview

Uploaded by

Table Of Contents:

Functions of Normal Skin:

Basic Structure of Normal Skin:

- The 5 Layers of the Epidermis:

o 2) Stratum Spinosum (Prickle Cell layer):

C = Corneum; L = Lucideum; G = Granulosum; S = Spinosum; B = Basale

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

o Langerhans Cells – (In Stratum Spinosum):

Public domain; Available from: [Link]

o Epidermopoiesis (Epidermal Renewal):

o Desquamation (Shedding of the Skin):

- Dermal-Epidermal Junction (Stratum Basale: Basement Membrane):

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

- Structure of the Dermis:

Available from: [Link]

Scientific Figure on ResearchGate. Available from: [Link]

§ Glycosaminoglycans (GAGs) = Absorb water – Provide Viscosity

- Structure of The Hypodermis:

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

o Cutaneous Circulatory Apparatus – 2 Types of Vessels:

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

Creative Commons: By Cristina Sala Ripoll; University of Dundee;

OpenStax College, CC BY 3.0 <[Link] via Wikimedia Commons

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

CNX OpenStax, CC BY 4.0 <[Link] via Wikimedia Commons

Key words + Definitions:

Morphology Terminology – Primary Lesions:

Lesion Name: Lesion Description: Picture:

Erythroderma Red rash covering >90% of the Body

Telangiectasia Permanently dilated dermal blood vessels to the point of

Macule A macule is a small, flat is of altered colour, without

Patch A patch is a large Macule

Petechiae Tiny macules of blood in the skin; Small, non-blanching

Purpura A Large Macule or Patch of blood in the skin. Doesn’t

(The hallmark of vasculitis – severe inflammation of the

Micropapule A Very Small raised lesion 1-2mm in diameter.

Papule A small raised lesion (less than 0.5cm)

Plaque Flat-topped, raised area of the skin. (Usually dermal

Papilloma A nipple-like mass projecting from the skin

Burrow A linear Papule caused by a burrowing organism. Eg:

Nodule A raised, solid lesion greater than 0.5cm in width AND

Tumour A mass of enlarged tissues of more than 1cm diameter

Bulla A large Vesicle more than 0.5cm in diameter

Pustule A small Pus-filled vesicle of less than 5mm in diameter

Impetiginized Covered in Crust, Pustules, & Often Weeping

Cyst A cavity containing liquid, semisolid, or solid material

Abscess A Pus-containing cavity of more than 1cm in diameter.

Fissure A deep crack - extends down to the dermis & blood

Erosion A superficial incomplete loss of the epidermis. Eg:

Ulcer An area of complete loss of the epidermis and often

Wheal A wheal is an elevated, white, compressible area

Angioedema Oedema which extends to the subcutaneous tissue

Comedone A plug of keratin or sebum blocking a sebaceous orifice

Alopecia Can be:

Eschar Patch of Dead Skin (necrosis) – A Thick Crust over an

Lesion Name: Lesion Description: Picture:

Keratosis Thickening of the skin. Eg: Solar Keratosis

Hyperkeratosis Large are of Thickened skin → Thick Scale.

Verrucous Very Hyperkeratotic – Similar to a Wart

Lichenification Palpable epidermal thickening of the skin usually due to

Crust Dried serum, pus, or blood usually mixed with epithelial

Atrophy Thinning of the skin (epidermal, dermal, or

Ulcer An area of complete loss of the epidermis and often

Excoriation A superficial loss of epidermis from scratching or picking,

Scar A pale, firm raised or depressed lesion resulting from skin

Stria Streak-like, linear, pink/purple/white marks due to

Pigmentation An Increase or Decrease in skin pigmentation. Eg:

- Relating to Edge of Rash:

Creative Commons: [Link]

Creative Commons: [Link]

Creative Commons: [Link]

Public Domain: Serephine, CC0, via Wikimedia Commons

Mohammad2018, CC BY-SA 4.0 <[Link] via Wikimedia Commons