Dermatology 206 Notes and Summary PDF

ATOLOGY 2 RM 06 DE NOTES AND SUMMARY Defenitions Acute Disease - An acute disease has a rapid onset, with symptoms that appear and change quickly. These symptoms can be intense and are of short duration. Allergy- A sensitized person...

ATOLOGY 2 RM 06 DE NOTES AND SUMMARY Defenitions Acute Disease - An acute disease has a rapid onset, with symptoms that appear and change quickly. These symptoms can be intense and are of short duration. Allergy- A sensitized person may develop an allergic reaction to typically harmless substances upon contact with an allergen. The immune response can be indicative, with symptoms including a pruritic rash, inflammation, hay fever symptoms, and severe reactions such as anaphylactic shock. Common signs of an allergic reaction are not confined to the product application area, often lack clear boundaries, and do not subside after the allergen is removed. Chronic Disease - A chronic disease is a long-lasting condition that develops over time and may worsen but tends to occur in recurring episodes. Congenital Disease - Congenital diseases can be passed on through direct contact. Diagnosis - Diagnosis involves the recognition of a disease based on its symptoms. Epidemic- An epidemic refers to a disease that attacks a large number of people simultaneously in a specific locality. Erythematous - Erythematous describes skin and/or mucous membranes that exhibit abnormal redness due to an inflammatory response. Etiology/Aetiology - Etiology is the study of the causes or sets of causes of a disease or condition. Eudermic - Eudermic refers to substances that are skin-friendly and non-irritating. Infectious Disease- Infectious diseases are caused by pathogenic microorganisms such as bacteria, viruses, parasites, or fungi. These diseases can spread directly or indirectly. Inflammation - Inflammation is an immune response characterized by redness, pain, itching, swelling, and heat. It can be acute or chronic and may be localized or a result of injury, irritation, or infection. Occupational Disease- Occupational diseases are caused by certain types of employment, such as dermatitis from contact with chemicals, hearing loss from high noise levels, and eye diseases from specific lighting. Pandemic- According to the WHO, a pandemic is a new disease that spreads worldwide with little to no resistance from hosts or medications. Parasitic Disease- Parasitic diseases are caused by fungal or animal parasites. Pathogenic Disease - Pathogenic diseases result from organisms that produce illness, such as bacteria, viruses, fungi, or protists. Pathology - Pathology is the study of diseases and their effects. Porphyria - Porphyria refers to a group of hereditary diseases that affect the skin or nervous system due to abnormal metabolism of hemoglobin. Extreme sensitivity to sunlight and poor healing ability are characteristic of porphyria cutanea tarda, the most common type of porphyria. Prognosis - Prognosis involves predicting the probable course and duration of a disease. Pruritic- Pruritic describes a skin sensation that compels the individual to scratch. Seasonal Disease- Seasonal diseases are influenced by weather changes throughout the year.  Skin Disease - A skin disease is characterized by an infection affecting the skin and is often associated with objective signs. Systemic Disease- A systemic disease involves the under- or over-functioning of internal glands and affects the body and its systems as a whole. Trichology- Trichology is the study of hair. Venereal Disease- Venereal diseases are contagious infections acquired through sexual relations with an infected person. Topography of the skin Topography of the skin refers to its texture and the various components that create its unique surface on different parts of the human body. Purpose and function : The thickness of the skin varies depending on its function in different areas of the body. It ranges from 0.2 cm to 0.05 cm, being thickest on the palms of the hands and the soles of the feet, and thinnest on the eyelids and lips. The thickness of the skin is directly linked to its role in protection and its ability to manage mechanical stress. The smoothness of the skin determines its stretchability in specific areas. For example, the skin on the face is not meant to stretch and change positions constantly, which is why it is smoother and has a smaller surface area. In contrast, the elbows have furrows that allow for additional folds of skin and greater mobility. Skin tension also affects its mobility across different parts of the body. It is firm and taut over flat, bony structures but flaccid over the joints. The ridges (hills) and sulci (valleys/depressions) create fingerprints on the palmar surface of the fingers and toes. A single depression in the skin is referred to as a sulcus cutis, and this textural characteristic offers multiple benefits, such as increasing surface area, providing space for more tactile sensory organs, and enhancing grip. Without elasticity and the ability to retract, the skin would not be able to adapt to body movements or adjust to changes in the size or position of underlying structures. Pigmentation plays a protective role and can indicate certain systemic diseases. The vascular network is essential for feeding the skin and ensuring cellular metabolism occurs; without it, the skin can become necrotic. Hair contributes to the skin's protective nature, temperature management, and mechanical protection. Scarring occurs when the skin is damaged due to trauma or infection, which alters the texture of the skin. Wound healing and scarring As somatologists, we can combine several treatment options to achieve a positive result. A marked improvement can be made at the somatology level, but complete erasure of any scar is unlikely. Wound Healing Cascade Consists of four phases initiated and controlled by specific growth factors (peptides). Growth factors are biologically active substances that affect cellular functioning, growth, and metabolism. Phases of Wound Healing Phase 1: HAEMOSTASIS 1. Blood vessels constrict to slow down bleeding. 2. This process is stimulated by platelets exposed to oxygen, which then clump together to form a plug over the wound.  3. Blood clotting proteins release thrombin, an enzyme that converts fibrinogen to fibrin, forming a fibrin clot. 4. Mast cells degranulate, releasing histamine, which increases cellular permeability. 5. Growth factors promote blood coagulation. Phase 2: Inflammation 1. After the wound is closed, capillaries enlarge due to stimulation by growth factors. 2. Fluids accumulate in the damaged area, providing increased nutrients, oxygen, and blood plasma, including white blood cells (WBCs). 3. Macrophages in the area clean out the wound by performing phagocytosis on cellular debris. 4. These macrophages produce chemical substances known as growth factors, which aid in the repair of the wound. 5. The longer this stage takes, the longer the overall healing process will be. Phase 3: PROLIFERATION 1. In this phase, new cells are created. 2. Fibroblasts are stimulated by growth factors to produce collagen and elastin. 3. Fibroblasts synthesize collagen. 4. Matrix metalloproteinases (MMPs) help lay down new collagen to remodel the extracellular matrix (ECM) while breaking down old collagen or excess strands. 5. Collagenase, an enzyme associated with MMPs, is released to break down the peptide bonds in collagen. 6. Tissue inhibitors of metalloproteinases (TIMPs) inhibit collagenase, preventing it from breaking apart collagen strands. 7. If TIMPs are unable to effectively regulate collagenase, it may continue to break down healthy collagen produced by the MMPs, leading to excessive collagen production. Phase 4: REMODELING In this phase, immature collagen (type 3) is replaced by mature collagen (type 1). What Happens If Proliferation Does Not End? TIMPs fail to regulate the MMPs effectively. As a result, the formation of new collagen continues unchecked. This leads to the continuous development of new, immature collagen. Consequently, the extracellular matrix (ECM) expands, resulting in excessive tissue growth and the formation of hypertrophic scars. Conversely, if collagen production is insufficient, an atrophic scar may develop. Extended Inflammatory Phase - This phase results in a chronic wound, as the proliferation process cannot occur to facilitate complete healing. - Fibroblasts do not receive the signal to produce new collagen due to the continued activity of white blood cells (WBCs) in the area. - Tissue inhibitors of metalloproteinases (TIMPs) continue to break down collagenases, causing fibroblasts to produce increasing amounts of immature collagen, which creates a soft, "mushy" texture in the skin. - Without healthy collagen and new cells being generated, the wound remains "open." - The healing process cannot progress beyond this point until the inflammatory phase concludes. An epidermal wound closes through a process called epidermal migration, which is influenced by epidermal growth factor. In contrast, a dermal wound closes through collagenesis, which requires stimulation of fibroblasts by fibroblast growth factor, among other cellular components. Dermal wounds can have complications that arise from either excessive or insufficient collagen production by the fibroblast cells. Scarring is a natural outcome of the wound healing process. The type, depth, and size of a scar depend on which regions of the skin have been damaged, leading to dermal inflammation. A scar alters the topography of the skin and may result in the loss of certain characteristics in the affected area. If collagenesis is not appropriately halted by tissue inhibitors of metalloproteinases (TIMPs), an excess of immature collagen may accumulate, leading to the formation of surplus cellular tissue in the wound area. This condition results in a hypertrophic scar, which is characterized by excessive collagen deposition and a decrease in collagenase activity. When the scar extends beyond the borders of the original wound, it is referred to as a keloid scar. An atrophic scar results from inadequate collagen production following cellular injury. Three common post acne scars 1. Ice Pick Scars Appearance: Deep, narrow, and pitted. Cause: Severe acne that penetrates deep into the skin. Treatment: Difficult to treat; may need deep chemical peels, microneedling, or punch excision. 2. Boxcar Scars Appearance: Broad, shallow-to-medium depressions with sharp edges. Cause: Inflammatory acne that destroys collagen. Treatment: Microneedling, laser resurfacing, or dermal fillers can help. 3. Rolling Scars Appearance: Wide, wave-like depressions with smooth edges. Cause: Damage beneath the skin surface, often due to long-term inflammation. Treatment: Subcision, microneedling, or laser treatments work well. The depth of the wound will directly determine which regions are involved , with each region a diffrent cellular response can be expected for wound healing to take place Why is Scar Prevention Key in Acne Treatment? preventing scarring is more effective than trying to treat scars after they form. Here are some important steps to consider: Manage Inflammation Early- Addressing inflammation promptly can minimize skin damage. Avoid Picking or Popping Lesions-This can lead to further irritation and increased risk of scarring. Use Ingredients That Promote Healthy Skin Healing-Incorporate products that support the skin's natural healing process. Topical Treatments: Topical Retinoids- These help increase cell turnover, unclog pores, and stimulate collagen production. They are effective for preventing scarring and treating post-inflammatory hyperpigmentation (PIH) as well as mild atrophic scars. Silicone Gels/Sheets- These are primarily used for hypertrophic scars and keloids. They help flatten and soften raised scars while also reducing redness. Chemical Peels- These treatments exfoliate the skin using acids, promoting skin renewal and helping to improve its overall appearance. Extra Benefits of Scar Treatments: Fibroblast Stimulation: Promotes collagen production. Glycosaminoglycans (GAGs) Stimulation: Increases hydration and elasticity. Mechanical Resurfacing Techniques: Dermabrasion A medical-level, deeper mechanical exfoliation. Often performed under anesthesia; ideal for severe scarring. Microdermabrasion A more superficial treatment that removes the stratum corneum. Suitable for maintenance purposes but not effective for deep scars. Laser and Radiofrequency (RF) Treatments: Ablative Lasers (e.g., CO₂, Er:YAG) Remove the top layers of skin. Stimulate new collagen production and help resurface deeper scars. Involves longer downtime. Non-Ablative Lasers Work deeper in the skin without removing surface layers. Stimulate collagen over time. Less downtime required, but may need more sessions for optimal results. Fractional Laser Treats "fractions" of the skin by creating micro-columns of damage surrounded by healthy skin. Balances effective results with faster healing. Punch Techniques Used for deep ice pick or boxcar scars. Punch Excision: The scar is surgically removed and stitched up. Punch Elevation: The bottom of the scar is lifted and leveled with the surrounding skin. This can be done using laser or RF tools. Surgical and Fill Options: Subcision A needle is used under the skin to break fibrotic bands that are pulling down the scar. Stimulates healing and collagen production. Dermal Grafting Skin is taken from another area and placed into the scar. Best for deep or wide scars. Tissue Augmentation Fillers such as hyaluronic acid or fat transplants are used to lift indented scars for a smoother appearance. Results can be temporary (6-18 months) or semi-permanent depending on the filler. Microneedling Tiny needles (0.5–2.5 mm) create micro-injuries to trigger collagen production. Safe for all skin types, including darker skin tones. Lower risk of post-inflammatory hyperpigmentation (PIH). Depth of treatment depends on the scar type: 0.5 mm for pigmentation 1.5–2.5 mm for deeper scars Combination Therapy Example treatments include: Microneedling + PRP (platelet-rich plasma) TCA CROSS + Laser for stubborn scars Using multiple treatments together often yields better results. Recap Strategy: Classify scars as either: Atrophic (Indented)**: Ice pick, rolling, or boxcar scars—best treated with collagen-stimulating techniques. Hypertrophic/Keloid (Raised)**: Best treated with silicone, steroid injections, or laser therapies. Types of Acne Acne Conglobata Acne Conglobata primarily affects males due to their oily skin and enlarged sebaceous glands. The typical lesions consist of nodules that can lead to severe scarring, often resulting in ice-pick scars. This type of acne usually appears in early puberty and can worsen over the years as a result of hormonal activity. It is more common in individuals with fair skin and is typically found on the back, buttocks, and thighs. Post-Adolescent Facial Acne in Females: Pyoderma Faciale Pyoderma Faciale is a severe form of acne conglobata that exclusively affects women aged 20-30 years and is limited to the face. This condition may indicate underlying endocrine disorders, such as polycystic ovarian syndrome, hyperandrogenism, and thyroid disorders.  Comedones are rare in this condition; instead, it presents with densely clustered papules and numerous nodules. The entire face is covered with soft, tender lesions that drain yellow pus, and the skin appears intensely and diffusely red. Pyoderma Faciale is often preceded by emotional trauma and is associated with extreme facial oiliness. Acne Tropicalis This type of acne is similar to acne conglobata but has symptoms that are three times more severe. It is commonly found in moist or humid conditions, with an onset typically occurring around the age of 25 or older. Individuals usually have experienced mild acne before. Acne tropicalis tends to affect the trunk, face, buttocks, thighs, neck, and arms, and is extremely painful. Treatment generally involves a change of climate. Typical lesions include pustules, papules, and large nodules that may develop into draining sinuses. Acne Venenata Also known as contact acne, acne venenata occurs when a person is regularly in contact with certain substances. Pomade acne may develop from the application of various greases and oils to the scalp. Pomades, which are hair care products similar to wax, primarily cause this type of acne to manifest on the scalp, forehead, and temples. The characteristic features include open and closed comedones along with a few papules and pustules. Most pomades are comedogenic due to their ingredients. Acne venenata presents with pustules, inflammation, and underlying congestion that can form a vesicle-filled crust. Acne Cosmetica Acne cosmetica is related to acne venenata in its origins but differs in its appearance. This type of acne presents as underlying congestion with little to no inflammation, leading to an uneven skin surface. Comedogenic ingredients in cosmetics are contributing factors, and it may take up to six months for makeup to trigger this skin response. Acne Mechanica Acne mechanica is caused by mechanical stress and is usually located around the chin and collar area. Treatment involves reducing friction to alleviate symptoms. Acne Neonatorum Commonly known as infant acne, acne neonatorum appears two weeks after birth. It results from the baby’s direct exposure to fetal or maternal androgens. This type of acne presents as discrete, tiny smooth yellowish or whitish lesions primarily on the cheeks. It typically resolves by the age of five. GRADES OF ACNE GRADE 1 no inflammation, some comedones GRADE 2 some inflammation, papules, pustules GRADE 3 inflammation, papules, pustules, scarring GRADE 4 Inflammation, pain, papules, pustules, cysts, severe scarring Acne look-a-likes Peri-oral dermatitis Red rash that circles the mouth Skin can be scaly, dry and flaky with swollen papules Can be itchy and burns May spread to the nose and eye areas May return as rocsacea Woman between 25 and 45 who use topical steroids or face creams are at a higher risk Acne rosacea Redness, swollen small red, pus-filled bumps on the face. Commonly affects middle- aged women with fair skin. It can be mistaken for acne or other skin conditions React to a bacterium called bacillus oleronius. This causes the immune system to overreact. Folliculitis aka Barber’s rash Inflammatory disorder of the follicular and perifollicular skin resulting from in-grown hair due to hair removal Papules, pustules and post-inflammatory hyperpigmentation More frequent in African and Asian men because of the tight curly hair Keratosis pilaris This condition develops when the skin produces too much of a protein called keratin, which can block hair follicles and cause bumps to develop. The bumps are usually on the arms, thighs, cheeks and buttocks. They're white, sometimes red, and typically don't hurt or itch. Sebaceous hyperplasia Enlarged sebaceous glands. Small yellow bumps up to 3mm in diameter. Central hair follicle surrounded by yellowish lobules. Form of benign hair follicle tumour Prevalent in immunosuppressed patient e.g. following an organ transplant. Harmless and does not require treatment Cosmetic – removed by light electrocautery or laser vaporization Severe lesions – oral isotretinoin but lesions may recur. Ingrown hair / pseudofolliculitis Infection of the hair follicles Hair curves into the skin as it grows back after being removed by shaving or waxing Causes tiny, swollen bumps on the skin that may be painful. Small bumps that look like blisters or are filled with pus. Mainly affects darker skin with curly hair. Basal cell carcinoma Type of skin cancer which begins in the basal cells. Often appears as a slightly transparent bump on the skin Areas that are exposed to the sun, such as head and neck Caused by long-term exposure to UV rays Looks like a bump that’s skin colored or pink on lower Fitzpatrick skin. Looks like a bump that’s brown or glossy black and has a rolled border on higher Fitzpatrick skin. Plane warts Multiple small flat – topped skin-coloured papules. Face, hands and shines Caused by human papillomavirus HPV types 3 and 10 Seborrheic eczema aka seborrheic dermatitis Causes scaly patches and inflamed skin Patches of greasy skin covered with flaky white or yellow scales or crust Affects oily areas of the body such as the face, sides of the nose, eyebrows, ears, eyelids and chest Not contagious Can be itchy Pigmentary and its disorders Pigmentation disorders, also known as dyschromias, are pathological changes in the skin that can result in either hyperpigmentation or hypopigmentation (leukoderma). Dyschromia occurs due to malfunctioning melanocytes. Pigmentation refers to the coloring of the skin, primarily caused by melanin, a pigment produced by melanocytes in the epidermis. Hyperpigmentation is characterized by darkened areas of skin that arise when melanocytes deposit excessive melanin into the epidermal and/or dermal cells. Conversely, hypopigmentation or leukoderma occurs when melanin is diminished, absent, or never deposited in the skin. Hyperpigmentation: This is when patches of skin become darker than the surrounding area due to excess melanin production or melanin being trapped in the skin.  Hypopigmentation: This is when patches of skin become lighter than normal due to reduced melanin production or loss of melanocytes. Hyperpigmentation Lesions & Disorders Tan What it is: A temporary darkening of the skin after UV exposure. Cause: Sun exposure triggers melanin production as a natural protective response. Relevance: Can lead to sun damage and uneven skin tone over time. Ephelides (Freckles) What it is: Small, flat, light-brown spots usually on sun-exposed areas. Cause: Genetic predisposition and sun exposure. Relevance: Common in lighter skin types; no increase in melanocytes—just more melanin produced. Stains (Dermal Pigmentation) What it is: Flat, pigmented patches that don’t fade over time. Cause: Often result from post-inflammatory pigmentation or certain injuries. Relevance: Harder to treat as pigment is deeper in the skin (dermis). Lentigo (Liver Spots / Age Spots) What it is: Brown or black spots commonly found on aging or sun-exposed skin. Cause: Long-term UV exposure and aging. Relevance: Not harmful but can be a sign of photoaging. Melasma What it is: Symmetrical brown patches, often on the face. Cause: Hormonal changes (pregnancy, birth control), sun exposure, genetic factors. Relevance: More common in women; can be persistent and triggered by UV. Ochronosis What it is: A bluish-black discoloration, usually where skin-lightening products are used. Cause: Long-term use of hydroquinone or certain phenol-containing products. Relevance: Rare but difficult to treat; highlights risks of incorrect skin-lightening. Hypopigmentation Disorders Pityriasis Alba What it is: Pale, scaly patches—often on the face of children and teens. Cause: Thought to be related to eczema or dry skin. Relevance: Benign and self-limiting; improves with moisturising and mild steroid creams. Vitiligo What it is: White patches due to complete loss of pigment. Cause: Autoimmune destruction of melanocytes. Relevance: Can affect confidence/self-image; unpredictable progression. Albinism What it is: Genetic condition causing little or no melanin production. Cause: Inherited genetic mutation affecting melanin synthesis. Relevance: Affects skin, hair, and eye color; people with albinism are very sun-sensitive and at risk of skin cancers. Main types of vitiligo FOCAL a small isolated lesion in one specific area of the body SEGMENTAL on one side of the body, spreads rapidly, then pauses and can remain unchanged for years Can develop into mixed vitiligo NON-SEGMENTAL/GENERALISED Various parts of the body Acro-facial vitiligo Vitiligo Vulgaris Vitiligo universalis Other: Contact or occupational vitiligo