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COMPLETE LECTURE: Dermatology Pages 481-486 (First Aid / Pathology Review)

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PAGE 481: SYSTEMIC SCLEROSIS (SCLERODERMA)

What is Systemic Sclerosis?

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Line: "Triad of autoimmunity, non-inflammatory vasculopathy, and collagen deposition"

1. Autoimmunity - The immune system makes antibodies (special proteins usually meant to fight germs) that instead attack the body's own tissues. Like a soldier shooting his own teammates.
2. Non-inflammatory vasculopathy - "Vaso" = blood vessels, "pathy" = disease. The blood vessels get damaged and thickened - but WITHOUT inflammation (without the usual redness and swelling). The walls of the tiny blood vessels thicken and the tube inside narrows. Less blood reaches tissues.
3. Collagen deposition - Collagen is the main structural protein in our body, like the "cement" or "framework." Normally it holds tissues together. In scleroderma, too much collagen is laid down everywhere - in skin, lungs, kidneys, heart, gut. This makes organs stiff and hard.

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Line: "Commonly sclerosis of skin, manifesting as puffy, taut skin - without wrinkles"

• Sclerosis = hardening/thickening
• The skin becomes puffy first (like swelling), then gets taut (tight, stretched, shiny)
• Because the skin is so tight and stiff, wrinkles disappear - the face looks smooth but in an unhealthy way. Patients cannot open their mouth wide. Fingers become sausage-like.

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Line: "Fingertip pitting - can involve other systems: eg renal, pulmonary, cardiovascular, GI"

• Fingertip pitting = small pit marks/scars on the fingertips from tiny areas of tissue death (because blood supply is poor)
• The disease does NOT stop at skin. It can affect:
  • Renal = kidneys (can cause kidney failure)
  • Pulmonary = lungs (scarring, pulmonary hypertension - high pressure in lung blood vessels)
  • Cardiovascular = heart and blood vessels
  • GI = gut/gastrointestinal tract (difficulty swallowing, heartburn, poor movement of food)

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Line: "ACE inhibitors, heartburn, pulmonary interstitial fibrosis, pulmonary HTN, GI"

• ACE inhibitors = drugs (like enalapril) used specifically to treat scleroderma kidney crisis
• Heartburn = the food pipe (esophagus) gets stiff and cannot push food down properly, stomach acid refluxes up
• Pulmonary interstitial fibrosis = the lung tissue (interstitium = the "filling material" between air sacs) gets scarred and fibrous. The lungs become stiff, patient feels breathless
• Pulmonary HTN = pulmonary hypertension = high blood pressure in the blood vessels supplying the lungs. This strains the right side of the heart.

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Line: "75% female, 2 major types"

• Scleroderma affects women 3 times more than men - this is because autoimmune diseases in general prefer females (hormonal reasons)
• There are 2 main types - explained below

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DIFFUSE SCLERODERMA

Line: "Widespread skin involvement, rapid progression, early visceral involvement"

• Diffuse = widespread, all over
• Skin tightening covers large areas of the body - trunk, face, arms, legs
• Rapid progression = gets worse quickly
• Early visceral involvement = "visceral" means internal organs. So organs (lungs, kidneys, heart) are affected early in the disease, not after years

Line: "Associated with anti-RNA polymerase III antibody (anti-DNA topoisomerase-I antibody)"

• These are antibodies (immune proteins) that are found in the patient's blood
• Think of them as fingerprints of the disease - their presence helps doctors confirm the diagnosis
• Anti-Scl-70 (anti-DNA topoisomerase-I) is the classic antibody for diffuse scleroderma
• Anti-RNA polymerase III is associated with renal crisis risk

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LIMITED SCLERODERMA

Line: "Limited skin involvement confined to fingers and face"

• "Limited" here literally means the skin involvement is LIMITED only to the hands (fingers) and face
• Less widespread than diffuse type
• Progresses more slowly
• But can still develop serious complications over time (especially lung involvement called pulmonary arterial hypertension)

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CREST SYNDROME (a form of limited scleroderma)

Line: "Anti-centromere antibody. More benign clinical course"

• Anti-centromere antibody = the specific antibody (blood test marker) found in CREST/limited scleroderma
• Centromere = a part of the chromosome (your DNA bundle). The immune system wrongly makes antibodies against it
• "More benign clinical course" = compared to diffuse scleroderma, CREST progresses more slowly and is less dangerous (though not completely harmless)

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PAGE 481 (RIGHT SIDE): SKIN LAYERS

Line: "Skin has 3 layers: epidermis, dermis, subcutaneous fat (hypodermis, subcutis). Epidermal layers: come, let's get sunburned"

• Dermis = middle layer, contains collagen, blood vessels, nerves, hair follicles, sweat glands
• Hypodermis/Subcutis = deepest layer, mostly FAT. Acts as a cushion, insulator, and energy store

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PAGE 482: EPITHELIAL CELL JUNCTIONS

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TIGHT JUNCTIONS (Zonula Occludens)

Line: "Tight junctions (zonula occludens) - prevents paracellular movement of solutes, composed of claudins and occludins"

• "Zonula" = belt-like ring, "occludens" = occlude = seal/close
• Imagine these as a TIGHT SEAL or ZIPPER between cells
• They prevent substances from leaking between cells (paracellular = "para" = beside/between cells)
• For example, in the gut, tight junctions prevent toxic substances from slipping between gut lining cells into the bloodstream
• Claudins and occludins = the actual protein molecules that form this seal. Like the individual teeth of a zipper

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ADHERENS JUNCTIONS (Zonula Adherens)

Line: "Adherens junction (belt) - forms 'belt' connecting actin cytoskeletons of adjacent cells with cadherins"

• "Adherens" = adhering = sticking together
• These form a belt-like ring that goes around the cell
• They connect to the cell's internal actin cytoskeleton - "actin" is a protein that forms the internal scaffold of the cell (like an internal frame)
• Cadherins = the actual proteins that cross the gap and attach cells together. "Ca" = they need Calcium to work. This is important!
• E-cadherin specifically - when this is lost (as in cancer), cells can break free and spread = metastasis (cancer spreading to other organs). That's why the book says "E-cadherin promotes metastasis" is FALSE - loss of E-cadherin PROMOTES metastasis

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DESMOSOMES

Line: "Desmosome (spot) - structural support via intermediate filaments. Autoantibodies to desmoglein → pemphigus vulgaris"

• Desmosomes = "desmo" = bond, "soma" = body. These are SPOT-like connections - like rivets or spot welds between cells
• Instead of a belt (like adherens junctions), these are scattered individual spots
• They connect to intermediate filaments (keratin in skin cells) = these are stronger, more rigid than actin. Like reinforced steel rods
• Desmoglein = the specific protein that forms the desmosome connection across cells
• Pemphigus vulgaris = a serious blistering skin disease. The patient's immune system makes autoantibodies (antibodies against self) against desmoglein. When desmoglein is destroyed, skin cells separate from each other - this is called acantholysis. The result is large, painful blisters that break easily. The blisters are "bullous" (bulla = blister > 1cm)
• Key test: Nikolsky sign = when you rub the skin, the top layer slides off even on normal-looking skin

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GAP JUNCTIONS

Line: "Gap junction - channel proteins called connexons permit electrical and chemical communication between cells"

• Gap junctions are like tiny tunnels connecting neighboring cells directly
• Connexons = the proteins that form these tunnel channels
• Through these tunnels, ions (charged particles), small molecules, and even electrical signals can pass directly from one cell to the next - WITHOUT going outside the cell
• This is extremely important in the HEART - cardiac muscle cells use gap junctions to pass electrical signals rapidly, so the whole heart beats in a synchronized wave
• Also important in smooth muscle (gut, blood vessels) for coordinated contraction

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HEMIDESMOSOMES

Line: "Hemidesmosomes - connects keratin in basal cells to underlying basement membrane. Autoantibodies → bullous pemphigoid. (Hemidesmosomos are down 'bellow')"

• "Hemi" = half. These are like HALF desmosomes
• They anchor skin cells (at the base) to the basement membrane - the foundation layer the skin sits on
• Basement membrane = a thin sheet of proteins that sits between the epidermis and dermis. It's like the foundation of a building
• Bullous pemphigoid = another blistering disease where autoantibodies attack the hemidesmosome proteins (specifically BP180 and BP230)
• When hemidesmosomes are destroyed, the epidermis detaches from the basement membrane - creating tense (tight) blisters
• KEY DISTINCTION: Pemphigus vulgaris = blisters WITHIN the epidermis (intraepidermal), flaccid blisters. Bullous pemphigoid = blisters BELOW the epidermis (subepidermal), tense blisters. "Pemphigoid is below" - the book's memory trick "bellow" = below!

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INTEGRINS

Line: "Integrins - maintain integrity of basolateral membrane by binding to collagen, laminin, and fibronectin in basement membrane"

• Integrins = proteins that INTEGRATE the cell with its surrounding matrix
• They span the cell membrane and connect the inside of the cell to the extracellular matrix (ECM = the protein mesh surrounding cells)
• Collagen, laminin, fibronectin = the main proteins in the basement membrane / ECM. Collagen = strength, laminin = cell adhesion scaffold, fibronectin = helps cells stick
• Integrins are bidirectional signals - they tell the cell what's happening outside, and the cell can tell integrins to either grip tighter or let go

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EXOCRINE GLANDS

Line: "Glands that produce substances other than hormones (vs endocrine glands, which secrete hormones) that are released through ducts to the exterior of the body"

• Endocrine glands = secrete hormones DIRECTLY into the bloodstream (no ducts). Example: thyroid gland, adrenal gland
• Exocrine glands = secrete products through DUCTS to the outside world or to body surfaces. Examples: sweat glands, salivary glands, sebaceous (oil) glands, mammary glands

Three types of secretion:

• Products are packed into vesicles (little sacs) and released by exocytosis (the vesicle fuses with the cell membrane and pours out contents)
• The CELL IS NOT DAMAGED
• Example: Sweat glands, salivary glands, pancreas
• "Secretory vesicle" = the little pouch carrying the product

• A "pinched off" portion of the cell membrane buds off carrying products with it
• The cell loses a small part of its cytoplasm (cell contents) but survives
• Example: Apocrine sweat glands (in armpits, groin - these produce the sweat that bacteria act on to make body odor), mammary glands
• Image shows "pinched portion of cell" budding off

• The ENTIRE CELL disintegrates/dies and becomes the secretion
• "Holo" = whole - the whole cell is sacrificed
• Example: Sebaceous (oil) glands in skin - the entire cell fills with lipid and then bursts to release oily sebum
• The cell is shown "disintegrating" entirely
• Sebum lubricates hair and skin

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PAGE 483: DERMATOLOGIC TERMS (MACROSCOPIC AND MICROSCOPIC)

Macroscopic (what you can see with naked eye) Lesion Terms

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MACULE

• Flat change in skin color, well-defined, < 1 cm
• No elevation, no depression - just a color change you can SEE but cannot FEEL as raised
• Like a freckle or a vitiligo patch (white area)
• Why important? If you describe it correctly, the diagnosis becomes clearer

PATCH

• Same as macule (flat color change) but > 1 cm
• Example: Vitiligo patches (large depigmented areas)

PAPULE

• Elevated solid skin lesion, < 1 cm
• You can FEEL it as raised. Like a small bump
• Example: acne, neurofibroma (benign nerve tumor), moles

PLAQUE

• Elevated solid skin lesion, > 1 cm (basically a large papule, or papules merging)
• Example: Psoriasis plaques (red raised areas with silvery scales on knees/elbows)

VESICLE

• Small fluid-containing blister, < 1 cm
• Contains clear fluid (serum)
• Example: Chickenpox (varicella) early lesions, shingles (herpes zoster)

BULLA

• Large fluid-containing blister, > 1 cm
• Example: Bullous pemphigoid, pemphigus vulgaris (the autoimmune diseases we discussed)

PUSTULE

• Pus-containing blister (pus = dead white blood cells + bacteria + tissue debris = yellow/white)
• Example: Acne (infected pimples), pustular psoriasis, impetigo (skin infection in children)

WHEAL

• Transient (comes and goes quickly) smooth papule or plaque
• Hives/urticaria = wheals. When you press them, they turn white (blanch)
• Caused by fluid leaking from blood vessels due to histamine release (from mast cells)

SCALE

• Flaking off of stratum corneum (the dead outer layer)
• Example: Psoriasis (thick silvery scales), eczema, dandruff

CRUST

• Dry exudate (dried secretions - serum, pus, blood that has dried on the skin surface)
• Example: Impetigo - "honey-colored crusts" on face of children. These form when the vesicles/pustules break and dry

ULCER

• Epidermal loss that goes down to expose deeper structures (dermis, muscle, bone, tendon)
• The skin has been completely eroded away
• Example: Arterial ulcer (from poor blood supply), decubitus ulcer (bed sore from pressure), leprosy

EROSION

• Partial or full loss of epidermis (the outer layer) but WITHOUT breaking through the basement membrane
• Shallower than an ulcer
• Can be seen in GERD (acid from stomach damaging esophagus lining), pemphigus vulgaris (blisters that break leaving erosions)

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Microscopic Terms (what you see under the microscope)

HYPERKERATOSIS

• Abnormal premature keratinization = increased thickness of stratum corneum (the outermost dead layer)
• The dead, keratinized layer is abnormally thick
• "Hyper" = increased, "kerato" = keratin, "osis" = condition
• Example: Callus on the sole (from friction), psoriasis, squamous cell carcinoma

PARAKERATOSIS

• Retention of nuclei in stratum corneum
• Normally, cells in the stratum corneum are dead and have NO nuclei. In parakeratosis, they still have nuclei = they are dying abnormally fast (the process was rushed)
• Like workers who left the building without clearing their desks
• Example: Psoriasis (very classic finding)

HYPERGRANULOSIS

• Increased thickness of stratum granulosum (the granule layer)
• Example: Lichen planus - the stratum granulosum is thickened. Lichen planus causes an itchy, flat-topped, purple papules - known for its 4 P's: Purple, Pruritic, Polygonal, Planar

SPONGIOSIS

• Epidermal accumulation of edematous fluid in intercellular spaces = "sponge" soaking up water
• Fluid collects BETWEEN cells in the epidermis, pushing them apart. Under microscope, the epidermis looks like a sponge
• Example: Eczematous dermatitis (eczema/atopic dermatitis) - the classic finding

ACANTHOLYSIS

• Separation of epidermal cells = cells lose their connections to each other
• "Acantho" = spiny layer (stratum spinosum), "lysis" = dissolution
• When desmoglein (the desmosome protein) is attacked by autoantibodies, cells lose grip and float apart
• Example: Pemphigus vulgaris - cells float apart within the epidermis

ACANTHOSIS

• Epidermal hyperplasia = increase in number of cells in stratum spinosum (the spiny layer)
• The spinosum layer becomes thickened
• Example: Acanthosis nigricans (dark, velvety patches in skin folds - seen in insulin resistance/diabetes, obesity), psoriasis

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PAGE 484: PIGMENTED SKIN DISORDERS

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ALBINISM

Line: "Normal melanocyte number with decreased melanin production due to decreased tyrosinase activity or defective tyrosine transport. Increased risk of skin cancer"

• Albinism = lack of pigment (white skin, white/blonde hair, pink/red eyes)
• The cells that MAKE pigment (melanocytes) are PRESENT - they are not missing
• But they CANNOT make melanin properly because:
  • Tyrosinase activity is decreased = the enzyme that converts tyrosine into melanin is not working well (this is the enzyme defect in most albinism)
  • OR tyrosine transport is defective = tyrosine (the raw material) cannot get into the cell
• Result: No pigment → skin has no UV protection → increased cancer risk (especially squamous cell carcinoma and melanoma)
• Also: vision problems (melanin is needed for eye development)

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MELASMA (CHLOASMA)

Line: "Acquired hyperpigmentation associated with pregnancy ('mask of pregnancy') or OCP use. More common in darker skin tones"

• Melasma = patches of darker skin, usually on the face (cheeks, forehead, upper lip)
• "Mask of pregnancy" = it looks like a mask on the face. Nicknamed this because it commonly appears during pregnancy
• Acquired = not present at birth, develops during life
• Why pregnancy? Estrogen and progesterone (pregnancy hormones) stimulate melanocytes to produce more melanin
• OCP = oral contraceptive pill - same hormones → same effect
• Darker skin = more melanocytes are active, so any stimulus causes more visible darkening

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VITILIGO

Line: "Irregular patches of complete depigmentation. Caused by destruction of melanocytes (believed to be autoimmune). Associated with other autoimmune disorders"

• Vitiligo = white/depigmented patches on skin, irregular edges
• Complete depigmentation = the patches have ZERO pigment. Pure white. This distinguishes vitiligo from albinism (albinism = reduced pigment everywhere, vitiligo = absent pigment in patches)
• Destruction of melanocytes = the pigment-making cells are being destroyed
• Autoimmune = the immune system attacks its own melanocytes. Think of it like friendly fire
• Associated with autoimmune disorders = patients with vitiligo are more likely to also have thyroid disease (Hashimoto's), type 1 diabetes, Addison's disease - all autoimmune. This makes sense as the underlying immune dysregulation affects multiple organs

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WAARDENBURG SYNDROME

Line: "Patchy depigmentation of skin, hair, and irises that can be associated with deafness. Caused by defects in the differentiation of neural crest cells into melanocytes"

• Waardenburg syndrome = a genetic condition
• Neural crest cells = during embryo development, special cells called neural crest cells migrate throughout the body and become many different cell types - including melanocytes (pigment cells) and cells in the inner ear (needed for hearing)
• When this migration or differentiation (becoming the right cell type) goes wrong:
  • Some areas lack melanocytes → white patches of skin, white streak of hair (poliosis), different colored eyes (heterochromia iridis)
  • Inner ear development is affected → sensorineural deafness (nerve deafness)
• Key feature: hearing loss + white forelock (streak of white hair) = think Waardenburg

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SEBORRHEIC DERMATITIS

Line: "Erythematous, well-demarcated plaques with greasy yellow scales in areas rich in sebaceous glands, such as scalp, face, and periocular region. Common in both infants (cradle cap) and adults"

• Erythematous = "erythro" = red. Red skin
• Well-demarcated = clear borders (you can clearly see where the rash starts and ends)
• Plaques = raised areas
• Greasy yellow scales = the classic hallmark. This distinguishes seborrheic dermatitis from psoriasis (psoriasis has dry, silvery scales)
• Sebaceous glands = oil glands in skin. "Seba" = sebum = oily secretion. The rash occurs where these glands are most dense: scalp, face (eyebrows, sides of nose, behind ears), chest
• Cradle cap = in babies, this presents as thick, yellow, greasy scales on the scalp. It looks alarming but is benign and usually resolves on its own

Line: "Extensive disease may be associated with HIV infection and Parkinson disease. Sebaceous glands are not inflamed, but play a role in disease development. Possibly associated with Malassezia spp."

• HIV = immune deficiency → seborrheic dermatitis can be severe and widespread
• Parkinson disease = the mechanism is not fully understood, possibly related to autonomic nervous system affecting sebaceous gland activity
• Malassezia = a yeast (fungus) that normally lives on our skin. In seborrheic dermatitis, it is thought to overgrow and trigger inflammation. This is why antifungals help treat it
• Treatment: Topical antifungals (like ketoconazole shampoo/cream) + glucocorticoids (steroid creams to reduce inflammation)

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PAGE 485: COMMON SKIN DISORDERS

ACNE

Line: "Multifactorial etiology - increased sebum/androgen production, abnormal keratinocyte desquamation, Cutibacterium acnes colonization of the pilosebaceous unit (comedones), and inflammation"

• Multifactorial = many causes working together
• Sebum = skin oil. Androgens (male hormones - present in both males and females) increase oil production. This is why acne peaks at puberty (androgens rise)
• Keratinocyte desquamation = "keratinocytes" are the main skin cells, "desquamation" = shedding. Normally dead cells shed off. In acne, this shedding is abnormal - dead cells plug the hair follicle pore
• Cutibacterium acnes (old name: Propionibacterium acnes) = bacteria that lives in hair follicles. When follicles are plugged and oily, these bacteria multiply and trigger inflammation
• Pilosebaceous unit = "pilo" = hair, "sebaceous" = oil gland. The unit = hair follicle + attached oil gland together. The plugging of this unit = comedone (blocked pore)
  • Open comedone = blackhead (pore is open, oxidized melanin makes it black)
  • Closed comedone = whitehead (pore is closed, white/flesh colored)
• Papules, nodules, cysts = progression from mild to severe acne. Nodules and cysts are deeper, more inflamed, and can scar
• Treatment: Retinoids (vitamin A derivatives - reduce oil, normalize shedding), benzoyl peroxide (kills bacteria), antibiotics (reduce bacterial count and inflammation)

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ATOPIC DERMATITIS (ECZEMA)

Line: "Pruritic eruption associated with ichthyosis vulgaris and other atopic diseases (asthma, allergic rhinitis, food allergies); increased serum IgE. Often appears on face in infancy and then on flexural surfaces in children and adults"

• Pruritic = "pruritus" = itch. Intensely ITCHY. So itchy it's called "the itch that rashes" because scratching causes the rash
• Atopic = tendency to develop allergic conditions. The "atopic triad" = eczema + asthma + allergic rhinitis (hay fever). Many patients have all three
• IgE = a type of antibody involved in allergic reactions. Elevated in atopic people
• Ichthyosis vulgaris = a skin condition where skin is very dry and scaly (like fish scales - "ichthyo" = fish). Associated with atopy
• Distribution by age:
  • Infants = face (especially cheeks)
  • Older children/adults = flexural surfaces = the INSIDES of joints = behind knees, inside of elbows, wrists, neck. "Flexural" because these areas flex (bend)
• Key microscopic finding = spongiosis (fluid between cells, as we discussed)

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ALLERGIC CONTACT DERMATITIS

Line: "Type IV hypersensitivity reaction secondary to contact allergen (eg, nickel, poison ivy, neomycin)"

• Type IV hypersensitivity = a "delayed-type" allergic reaction. Let's understand the types briefly:
  • Type I = immediate allergy (IgE-mediated, like anaphylaxis from peanuts) - happens within minutes
  • Type II = antibody attacks cells (like blood transfusion reaction)
  • Type III = antibody-antigen complexes deposit (like lupus nephritis)
  • Type IV = T-cell mediated, delayed (24-72 hours after exposure). No antibodies involved - instead, sensitized T-lymphocytes (white blood cells) attack the allergen on the skin
• Examples:
  • Nickel = jewelry, belt buckles → ear piercing reaction
  • Poison ivy = the classic contact dermatitis, extremely itchy linear streaks
  • Neomycin = an antibiotic ointment, ironically causes allergic reaction in some people
• The rash appears WHERE the substance touched the skin - great clue for diagnosis

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KERATOSIS PILARIS

Line: "Follicular-based papules from keratin plugging, most often on extensor surfaces of arms and thighs"

• Follicular = around hair follicles
• Keratin plugging = keratin (the tough protein) clogs the hair follicle opening
• Result = small, rough, red/skin-colored bumps like permanent "goosebumps"
• Extensor surfaces = back of the arms, front of thighs (the outer/straight side of limbs)
• Very common, very benign. Many people have it. Associated with atopic dermatitis and dry skin

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MELANOCYTIC NEVUS (MOLE)

Line: "Common mole. Benign, but melanoma can arise in congenital or atypical moles. Intradermal nevi are papular. Junctional nevi are flat macules"

• Nevus (plural: nevi) = mole. A collection of melanocytes (pigment cells)
• Types based on where the melanocytes cluster:
  • Junctional nevus = melanocytes at the junction of epidermis and dermis = flat, dark macule
  • Intradermal nevus = melanocytes within the dermis = raised papule, flesh-colored to brown
  • Compound nevus = both locations = slightly raised
• Melanoma = malignant (cancerous) tumor of melanocytes. Can arise from existing moles especially atypical or congenital (present from birth) ones
• ABCDE warning signs of melanoma: Asymmetry, Border irregular, Color variation, Diameter > 6mm, Evolution (changing)

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PSEUDOFOLLICULITIS BARBAE ("Razor Bumps")

Line: "Inflammatory reaction to hair penetrating the skin characterized by firm papules and pustules that are painful and pruritic. Commonly occurs near jawline as a result of shaving. More common with naturally curly hair"

• Pseudofolliculitis = "pseudo" = false/fake, "folliculitis" = inflammation of hair follicle. So it LOOKS like folliculitis but isn't a true infection
• What happens: when curly hair is shaved short, it curls BACK and re-enters the skin nearby. The body sees the hair as a foreign body and triggers inflammation
• Papules and pustules near the jawline, neck
• Razor bumps = the street name
• More common in people with tightly curled/coily hair (particularly African-Americans)
• Prevention: stop shaving, use electric razor, grow beard

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PSORIASIS

Line: "Papules and plaques with silvery scaling, especially on knees and elbows. Acanthosis with parakeratotic scaling (nuclei still in stratum corneum), Munro microabscesses. Increased stratum spinosum, decreased stratum granulosum"

• Psoriasis = chronic inflammatory skin disease. The immune system (T-cells) drives abnormal, rapid skin cell turnover
• Silvery plaques on knees and elbows = the classic presentation. Also on scalp, nails
• Acanthosis = thickened stratum spinosum (too many cells in the prickle layer - cells are dividing too fast)
• Parakeratosis = nuclei still present in stratum corneum (because cells are rushing through so fast they don't have time to complete normal differentiation and lose their nuclei)
• Munro microabscesses = tiny collections of neutrophils (a type of white blood cell) within the stratum corneum. Microscopic pus pockets. Characteristic of psoriasis
• Increased stratum spinosum = thickened (due to rapid proliferation)
• Decreased stratum granulosum = the cells skip this layer because they're dividing so fast

Line: "Auspitz sign - pinpoint bleeding spots from exposure of dermal papillae when scales are scraped off"

• Dermal papillae = tiny finger-like projections of the dermis that poke up into the epidermis (bring blood vessels close to the surface)
• In psoriasis, the overlying thinned epidermis sits very close to these vessels
• When you scrape off the scale, you remove that thin epidermis → tiny blood vessels are exposed → pinpoint bleeding = Auspitz sign (pathognomonic = specific to psoriasis)
• Associated with nail pitting (pits in the nail surface) and psoriatic arthritis (joint inflammation in ~30%)

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ROSACEA

Line: "Inflammatory facial skin disorder characterized by erythematous papules and pustules but no comedones. May be associated with facial flushing in response to external stimuli. Complications include ocular involvement, rhinophyma"

• Rosacea = chronic inflammatory condition of the face
• No comedones = KEY distinction from acne! Rosacea has papules and pustules on the face, but no blackheads or whiteheads
• Facial flushing/blushing triggered by: alcohol, hot drinks, spicy food, sun, heat, emotional stress
• Ocular involvement = dry, red, irritated eyes (ocular rosacea)
• Rhinophyma = "rhino" = nose, "phyma" = bulbous growth. The nose becomes enlarged, bumpy, red and bulbous (like W.C. Fields' nose). This is from sebaceous gland hyperplasia and fibrosis

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SEBORRHEIC KERATOSIS

Line: "Well-demarcated, verrucous, benign squamous epithelial proliferation of immature keratinocytes with keratin-filled cysts (horn cysts). Looks 'stuck on.' Leser-Trélat sign - rapid onset of multiple seborrheic keratoses, indicates possible malignancy (eg, GI adenocarcinoma)"

• Seborrheic keratosis = very common benign skin growth in older adults
• Verrucous = warty-looking, rough surface
• "Stuck on" = the classic description! Looks like someone took a brown/tan waxy plaque and stuck it onto the skin. It appears glued on, not growing from within
• Horn cysts = tiny keratin-filled cysts within the lesion (visible microscopically)
• Leser-Trélat sign = sudden appearance of MANY seborrheic keratoses in a short time. This is a paraneoplastic sign = a warning that something is wrong internally. Associated with GI adenocarcinoma (stomach/colon cancer). The theory: cancer cells secrete growth factors that stimulate these keratoses to suddenly multiply

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VERRUCAE (WARTS)

Line: "Warts; caused by low-risk HPV strains. Soft, tan-colored, cauliflower-like papules. Epidermal hyperplasia, hyperkeratosis, koilocytosis. Condyloma acuminatum on anus or genitals"

• HPV = Human Papillomavirus. Many strains exist:
  • Low-risk strains (HPV 6, 11) = cause benign warts (condyloma acuminatum on genitals, common warts on hands/feet)
  • High-risk strains (HPV 16, 18) = cause cervical, anal, oropharyngeal cancers
• Koilocytosis = the microscopic hallmark of HPV infection. "Koilo" = hollow. Infected cells have a CLEAR HALO around the nucleus (the nucleus looks like it's floating in a clearing). These are called koilocytes. Pathologists look for this to confirm HPV
• Condyloma acuminatum = genital/anal warts. "Acuminatum" = pointed. Soft, fleshy, cauliflower-like

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URTICARIA (HIVES)

Line: "Hives. Pruritic wheals that form after mast cell degranulation. Characterized by superficial dermal edema and lymphatic channel dilation"

• Urticaria = hives. Intensely itchy, red wheals (raised areas) that appear and disappear
• Mast cells = cells in the skin loaded with inflammatory granules (especially histamine)
• Degranulation = the mast cell pours out its granules = releases histamine and other mediators
• Histamine causes:
  • Vasodilation = blood vessels widen = skin turns red
  • Increased vascular permeability = fluid leaks from vessels into tissue = swelling (edema)
  • Nerve stimulation = itch
• Superficial dermal edema = fluid accumulating in the upper dermis = the raised wheal
• Lymphatic channel dilation = the lymph channels try to drain the extra fluid
• Triggers: allergens, drugs, infections, cold, pressure, emotion. In many cases the cause is never found (idiopathic)
• Treatment: antihistamines (block histamine receptors)

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PAGE 486: VASCULAR TUMORS OF SKIN

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ANGIOSARCOMA

Line: "Rare blood vessel malignancy typically occurring in the head, neck, and breast areas. Usually in older adults, on sun-exposed areas. Associated with radiation therapy and chronic postmastectomy lymphedema. Stewart-Treves syndrome - cutaneous angiosarcoma developing after chronic lymphedema. Hepatic angiosarcoma associated with vinyl chloride and arsenic exposures"

• Angiosarcoma = "angio" = blood vessel, "sarcoma" = malignant (cancerous) tumor of connective tissue
• Very aggressive cancer - hard to treat, detected late
• Risk factors:
  • Sun exposure (radiation damage to cells)
  • Radiation therapy (used to treat breast cancer, can later cause angiosarcoma in irradiated area)
  • Chronic lymphedema = long-standing swelling from blocked lymph vessels (e.g., after mastectomy = breast removal, lymph nodes removed → arm swells chronically)
• Stewart-Treves syndrome = angiosarcoma specifically arising in a chronically lymphedematous (swollen) arm after mastectomy
• Hepatic angiosarcoma (in liver) = associated with industrial exposure to:
  • Vinyl chloride = used in making PVC plastic
  • Arsenic = toxic metal (in pesticides, some water sources, old medications)
  • Also thorotrast (old radioactive contrast dye)

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BACILLARY ANGIOMATOSIS

Line: "Benign capillary skin papules found in patients with AIDS. Caused by Bartonella infections. Frequently mistaken for Kaposi sarcoma, but has neutrophilic infiltrate"

• Benign = not cancer
• Capillary skin papules = small red/purple raised spots
• AIDS patients = immunocompromised (immune system severely weakened by HIV). These opportunistic infections attack people whose immunity is down
• Bartonella = bacteria. Two species cause bacillary angiomatosis: Bartonella henselae (cat scratch fever organism) and Bartonella quintana
• Mistaken for Kaposi sarcoma = both look like red/purple skin papules in AIDS patients
• Key difference: bacillary angiomatosis has neutrophilic infiltrate (neutrophils = white blood cells that fight bacteria - present because this is a bacterial infection). Kaposi sarcoma has lymphocytic infiltrate (lymphocytes = different white blood cells)
• Treatment: antibiotics (it's bacterial, so it responds to antibiotics!)

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CHERRY ANGIOMA

Line: "Benign capillary hemangioma commonly appearing in middle-aged adults. Does not regress. Frequency increases with age"

• Cherry angioma = a benign collection of dilated capillaries in the skin. Named for their bright cherry-red color
• Small (1-5mm), bright red, dome-shaped spots
• Hemangioma = "hema" = blood, "angioma" = benign blood vessel tumor
• Appears from middle age onward; almost everyone has some by age 70
• Does not regress = once it appears, it stays (unlike infantile hemangioma which shrinks)
• No treatment needed (purely cosmetic)

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GLOMUS TUMOR

Line: "Benign, painful, red-blue tumor, commonly under fingernails. Arises from modified smooth muscle cells of the thermoregulatory glomus body"

• Glomus body = a specialized structure in the skin (especially fingertips, nail beds) that controls blood flow for temperature regulation. "Thermo" = temperature, "regulatory"
• It contains modified smooth muscle cells that can open/close blood flow rapidly to control heat loss
• When a tumor forms from these cells = glomus tumor
• Classic triad: tiny tumor under fingernail + exquisite pain (especially cold sensitivity) + point tenderness (press exactly on the spot = severe pain)
• Benign, treated by surgical removal → immediate relief

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KAPOSI SARCOMA

Line: "Endothelial malignancy most commonly affecting skin, mouth, GI tract, respiratory tract. Classically seen in older Eastern European males, patients with AIDS, and organ transplant patients. Associated with HHV-8 and HIV. Lymphocytic infiltrate, unlike bacillary angiomatosis"

• Endothelial = arising from endothelial cells = the cells lining blood vessels
• Malignant = cancer
• Purple/red-brown plaques and nodules on skin - can look like bruises initially
• Populations:
  • Classic KS: elderly Eastern European or Mediterranean males (rare, indolent = slow-growing)
  • AIDS-associated KS: most common in men who have sex with men; very aggressive, widespread
  • Transplant-associated KS: from immunosuppression
• HHV-8 = Human Herpesvirus 8 = the causative virus for ALL forms of Kaposi sarcoma. Without HHV-8, KS doesn't occur. HIV creates immune suppression that allows HHV-8 to drive KS
• Lymphocytic infiltrate = under microscope, lymphocytes (not neutrophils) surround the tumor. This distinguishes from bacillary angiomatosis (neutrophilic)

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PYOGENIC GRANULOMA

Line: "Polypoid lobulated capillary hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy"

• Pyogenic = "pyogenic" usually means pus-forming, but here it's a misnomer - NOT caused by infection, NOT really a granuloma
• It is actually a rapidly growing benign vascular tumor (capillary hemangioma)
• Polypoid = sticks out like a polyp on a stalk
• Lobulated = divided into round lobules
• It bleeds VERY easily and profusely when touched (thin-walled blood vessels with no protection)
• Triggers:
  • Trauma (minor injury triggers abnormal vascular growth)
  • Pregnancy = hormones (especially estrogen) stimulate its growth; pregnancy epulis = pyogenic granuloma on gum
• Treatment: excision (cutting it out) or cautery

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INFANTILE HEMANGIOMA

Line: "Benign capillary hemangioma of infancy. Appears in first few weeks of life (1/200 births); initially grows rapidly, then involutes starting at age 1. Infantile hemangiomas spontaneously involute; cherry angiomas cannot"

• Hemangioma = benign blood vessel tumor
• Very common in babies - 1 in 200 births
• "Strawberry hemangioma" = bright red, raised, soft, compressible tumor on skin
• Natural history - KEY SEQUENCE:
  1. Not present at birth (or faint mark)
  2. Appears in first few weeks of life
  3. Rapid growth in first year
  4. Involutes (shrinks) spontaneously starting around age 1, usually completely gone by age 5-7
• KEY DISTINCTION from cherry angioma: Infantile hemangioma INVOLUTES on its own. Cherry angiomas DO NOT. "Infantile hemangiomas spontaneously involute; cherry angiomas cannot."
• Most need no treatment. If large, causing vision problems, airway compromise, or ulceration → treat with propranolol (beta blocker that shrinks them)

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SUMMARY TABLE: Autoimmune Blistering Diseases (Important High-Yield)

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SUMMARY TABLE: Vascular Skin Tumors

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