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Nursing Field Notes / Skin & Wound · Integumentary Foundation · Anatomy & Physiology + Fundamentals
🩹 SKIN & WOUND SET NG-051 Skin (foundation) NG-044 Pressure Injuries NG-080 Wound Care NG-116 Frostbite NG-182 Dermatitis NG-225 Psoriasis NG-204 Skin Cancer

The Skin 🧬

Structure & function — the foundation page for the whole Skin & Wound set

NG-051 INTEGUMENTARY · FOUNDATION ADHD-friendly visual edition

Skin is not wrapping paper — it is the body's largest organ, about 1.5–2 m² of surface and roughly 15% of body weight. Every other page in this set (pressure injuries, wound care, frostbite, dermatitis, psoriasis, skin cancer) is a story about which layer got hurt and how deep it went. Learn this cross-section once and the rest becomes depth, not memorization.

📄 Simple Nursing original — opens in Drive →

3 layers, top → bottomEpidermis · Dermis · Hypodermis (subcutaneous). Then muscle & bone.
🛡️ SHIELDSensation · Heat control · Immunity · Excretion · Layer (barrier) · D vitamin.
Depth = severityEpidermis only = heals fast. Past the dermis = no skin appendages left to regrow from.
Describe, don't diagnoseChart the lesion morphology — flat? raised? fluid? size? — not "rash".
🧬

THE LAYERS

STEP 1 · STRUCTURE

One drawing to rule the whole set — memorize this cross-section and every later page is just "how deep did the injury go?"

Lecture slide showing eight primary skin lesion types in cross-section: macule, papule, vesicle, ulcer, nodule, pustule, plaque and fissure, each drawn through the skin layers.
From your lecture. The eight words every skin question is built from. Flat = macule. Raised and solid = papule. Fluid = vesicle. Pus = pustule. Deep and raised = nodule. Crack = fissure.

🔬 Master cross-section — full-thickness skin

FULL-THICKNESS SKIN · vertical cutaway surface at the top · muscle at the bottom · not to scale ① EPIDERMIS ② Dermo–epidermal junction ③ Sebaceous gland ④ Arrector pili muscle ⑤ DERMIS ⑥ Deep cutaneous plexus ⑦ Eccrine sweat gland ⑧ HYPODERMIS (subcutaneous) ⑨ Muscle · fascia · bone avascular · 4–5 strata · ~28-day turnover rete ridges — where blisters split sebum → keeps skin supple, slightly acidic stands the hair up = goosebumps, traps heat collagen + elastin, vessels, nerves, glands arteriole (red) + venule (blue) — the heat radiator spiral duct to a surface pore → cooling sweat fat = insulation, cushion, energy store the floor — Stage 4 injury reaches here hair shaft (dead keratin) Meissner · light touch Pacinian · deep pressure melanocyte · pigment free nerve endings
epidermis dermis fat artery vein nerve
🧠 Read it top to bottom like a sandwich: dry crust (epidermis) → the filling with everything living in it (dermis) → butter (fat) → the plate (muscle & bone). Every wound page in this set asks one question: how far into the sandwich did it go?

🧬 Epidermis — the barrier, and it has no blood supply

Avascular. It is fed by diffusion from the dermis below. That is why a shallow scrape oozes clear fluid instead of bleeding, and why the epidermis alone can regenerate perfectly with no scar.

  • Keratinocytes — 90%+ of the cells. Born at the bottom, pushed up, flatten, die, flake off. Full turnover ~28 days (faster in psoriasis — see NG-225).
  • Melanocytes — make melanin, which shields DNA from UV. Everyone has about the same number; skin tone reflects how much pigment they make.
  • Langerhans cells — the immune sentinels. They present antigen; they are the reason allergic contact dermatitis exists (NG-182).
  • Merkel cells — light touch / discriminative sensation, sitting on the basal layer.
🧠 Strata, deep → surface: Basale · Spinosum · Granulosum · Lucidum · Corneum = "Baby Skin Gets Less Cracked." Lucidum only exists on palms and soles.

🔬 Zoom: the strata, and the 28-day escalator

EPIDERMIS · magnified · deep (bottom) → surface (top) ~28 days born → pushed up → dies → sheds Corneum — dead keratin plates Lucidum — palms & soles only Granulosum — cells start to die Spinosum — desmosome "spines" Basale — the only dividing layer water-proof brick wall keratohyalin granules cells glued together here + melanocytes + Merkel cells destroy this = no regrowth 🟣 melanocyte 🟡 Merkel cell wavy line = dermo-epidermal junction
🧠 The basale is the nursery. If a burn, pressure injury or frostbite kills the basal layer across a whole area, that area cannot re-epithelialise from the surface — it must fill in from the edges or be grafted.

🧬 Dermis — the workshop where everything lives

This is the layer with the blood, nerves, glands and follicles. Injuries that reach it hurt, bleed and can scar.

  • Papillary dermis (thin, upper) — loose tissue + capillary loops that feed the epidermis; contains Meissner corpuscles.
  • Reticular dermis (thick, lower) — dense collagen (tensile strength) and elastin (recoil = turgor). Stretch it too fast and you get striae.
  • Holds the appendages: hair follicles, sebaceous glands, sweat glands — the cells that let partial-thickness wounds re-epithelialise from the middle outward.
  • Two vascular plexuses: a deep cutaneous plexus and a superficial subpapillary plexus — the body's heat radiator.
🧠 Collagen = rope, elastin = rubber band. Ageing loses the rubber band first — that is why the pinch test tents in older adults even when they are well hydrated.

🧬 Hypodermis — fat, insulation, and the drug depot

  • Adipose + loose connective tissue. Insulation, shock absorption, energy store, anchors skin to fascia.
  • Thickness varies enormously by site and body habitus — this is exactly why subcutaneous vs intramuscular injection depth is chosen by site and needle length.
  • Thin fat over a bony prominence = the classic pressure injury set-up (NG-044).
  • Poor perfusion here is why the cachectic, the very old and the very cold injure so fast.
🧠 Fat is the body's bubble wrap. Take the bubble wrap away (thin, malnourished, elderly) and every bone becomes a pressure point.

⭐ The appendages — three glands people constantly mix up

StructureEmpties intoSecretesWhereClinical hook
Eccrine sweat glandIts own pore on the skin surfaceWatery, salty sweatAlmost everywhere; densest palms, soles, foreheadThe real cooling system — evaporation. Lost fluid + Na⁺ + K⁺
Apocrine sweat glandThe hair follicleThicker, protein-rich fluidAxillae, groin, areolaeOdorless until skin bacteria digest it → body odor; activates at puberty
Sebaceous glandThe hair follicleOily sebumEverywhere except palms & soles; densest face, scalp, backBlocked + inflamed = acne. Keeps the surface supple and slightly acidic

Acid mantle: sebum + sweat keep the surface pH around 4.5–5.5. That acidity plus normal flora is real antimicrobial defense — which is why harsh soap, repeated scrubbing and incontinence-associated moisture all raise infection risk.

🧠 "Apocrine follows the hair, eccrine goes it alone." Sebaceous also drains into the follicle — so two of the three ride the hair.
🛡️

WHAT SKIN DOES

STEP 2 · FUNCTION

Six jobs. When you can name them, you can predict exactly what goes wrong when skin is lost.

🛡️ The six functions, drawn

SIX JOBS OF SKIN · each panel is the same cross-section ① BARRIER microbes out · water in break it = infection + fluid loss ② HEAT CONTROL sweat + vasodilate = lose heat vasoconstrict + goosebumps = keep heat ③ SENSATION touch · pressure · temp · pain Meissner · Pacinian · free endings neuropathy = injury you cannot feel → liver → kidney → active vit D ④ VITAMIN D needed to absorb Ca²⁺ → bone strength ⑤ IMMUNITY Langerhans cells catch antigen also why allergic contact dermatitis happens patch med ⑥ EXCRETE + ABSORB water · salt · urea out absorbs meds — and toxins
🧠 SHIELD — Sensation · Heat control · Immunity · Excretion & absorption · Layer (barrier) · D vitamin. Skin is a shield; a shield does six jobs.

🌡️ Thermoregulation — the two settings

❄️ COLD — hold the heat goosebump arterioles narrow pale, cool, shivering · sweat shuts off 🔥 HOT — dump the heat arterioles widen sweat flushed, warm, diaphoretic · fluid loss

Evaporation of sweat is what actually removes heat — sweat sitting on the skin does nothing until it evaporates. Humid air, occlusive dressings and heavy blankets all block it.

🧠 Cold = clamp down. Hot = open up. This one sentence explains pallor in shock, flushing in fever break, and the pale hard skin of frostbite (NG-116).

💥 What is lost when skin is lost

Every complication of a big wound or burn is just a function on this page failing:

  • Barrier gone → infection, then sepsis.
  • Water control gone → evaporative fluid loss, hypovolemia, hypothermia.
  • Protein leaves in exudate → low albumin → more edema → slower healing.
  • Heat control gone → the patient gets cold fast, especially in the OR or in an open wound.
  • Sensation gone → repeat injury goes unnoticed (diabetic foot, neuropathy).
🧠 Skin failing looks a lot like a leaky, unheated house with the front door open: things get in, heat and water get out.

⚠️ Who has fragile skin — flag these on admission

👵Older adultthin dermis, less fat
🍽️Malnourishedlow protein, low albumin
💧Incontinentmoisture macerates
🩸Poor perfusionPVD, shock, smoking
🍬Diabetesneuropathy + slow healing
💊Steroidsthin, atrophic skin
🛏️Immobilecan't offload pressure
🧠↓ Sensationwon't feel damage
🧠 "Thin, wet, starved, still, and can't feel it." Any two of those together and you should already be planning prevention.
🔎

LESION LANGUAGE

STEP 3 · DESCRIBE IT

"Rash" is not an assessment. These nine words are the vocabulary every derm question is written in.

🔎 PRIMARY lesions — the first thing the skin does

PRIMARY LESIONS · cross-section (side view) with the skin surface at the top MACULE flat · color change only < 1 cm · freckle, petechia > 1 cm = PATCH (vitiligo) PAPULE solid · raised · you can feel it < 1 cm · mole, wart, acne bump > 1 cm & flat-topped = PLAQUE PLAQUE raised · flat-topped · broad > 1 cm · psoriasis, eczema think "a plateau, not a hill" NODULE solid · DEEPER than a papule > 1 cm · lipoma, cyst felt more than seen VESICLE raised · CLEAR fluid < 1 cm · herpes, poison ivy > 1 cm = BULLA (burn blister) BULLA a big vesicle > 1 cm · friction / burn blister splits at the rete ridges PUSTULE raised · PUS inside acne, impetigo, folliculitis pus ≠ always infected (psoriasis) WHEAL raised · edema · TRANSIENT hives, allergic reaction, TB test itchy · moves & fades in hours
🧠 Sort by three questions in order: Is it raised? Is there fluid? Is it bigger than 1 cm? Flat → macule/patch. Raised & solid → papule/plaque/nodule. Raised & fluid → vesicle/bulla/pustule. Raised & it disappears → wheal.

🔎 SECONDARY lesions — what happens next (scratching, healing, breaking down)

SECONDARY LESIONS · depth of loss increases left → right SCALE flakes of dead keratin shedding psoriasis, dandruff CRUST dried serum, blood or pus = a scab impetigo, healing scrape EXCORIATION linear scratch marks self-inflicted the fingerprint of itch EROSION epidermis only lost moist, does NOT scar a popped vesicle ULCER through epidermis AND into dermis → WILL scar pressure injury, venous ulcer FISSURE deep linear crack dry, painful heel, angle of mouth

Also learn: lichenification = thickened, leathery skin with exaggerated skin lines from chronic rubbing (the hallmark of long-standing atopic dermatitis — NG-182); atrophy = thin, translucent, "cigarette paper" skin (chronic topical steroids); scar = fibrous replacement tissue; keloid = scar that grows past the original wound edges.

🧠 Erosion vs ulcer = the scar question. Erosion stops at the epidermis and heals invisibly. Ulcer breaches the dermis, so it heals with a scar. Same rule underneath pressure-injury staging.

🚨 The blanching test — the one that separates benign from serious

Press a red area with your finger, then release.

  • Blanches (turns white, then re-reddens) = blood still inside vessels. Reactive hyperemia, mild erythema, sunburn.
  • Does NOT blanch = blood has leaked outside the vessels, or tissue is already damaged. Non-blanchable erythema over a bony prominence is a Stage 1 pressure injury (NG-044).
  • Non-blanching pinpoint red-purple spots = petechiae; larger flat patches = purpura; a big bruise = ecchymosis. Petechiae + fever is an escalate-now finding.
🧠 "Blanches = blood behaving. Doesn't blanch = blood escaping."

📝 How to describe a lesion so it counts as charting

Use the same six slots every time and you can chart any skin finding:

  • Type — macule, papule, vesicle, ulcer…
  • Size — measure in cm (length × width × depth), never "the size of a quarter"
  • Color — and whether it blanches
  • Location — anatomical landmark, and left/right
  • Configuration — linear, annular (ring), grouped/clustered, target/iris, serpiginous
  • Distribution — localized vs generalized, flexural (eczema) vs extensor (psoriasis), dermatomal (shingles), sun-exposed
🧠 Chart it like a police report: what, how big, what color, where, in what pattern. "Rash to arm" tells the next nurse nothing.
🩺

ASSESS & PROTECT

STEP 4 · TECHNIQUE

Inspection, palpation, and the traps — especially in darker skin and in older adults.

🩺 Three bedside tests, drawn

① SKIN TURGOR pinch over sternum or clavicle snaps back <2s NORMAL — immediate recoil TENTS DEHYDRATED — stays tented ② CAPILLARY REFILL press nail bed 5 s, release, count press → it blanches < 3 seconds = adequate perfusion > 3 s = poor perfusion, cold, shock, PVD ③ BLANCH TEST on redness over a bony prominence turns white BLANCHES → reactive hyperemia stays red DOESN'T BLANCH → Stage 1 injury
🧠 Three fingers, three answers: pinch = hydration, press the nail = perfusion, press the redness = tissue damage.

⭐ Assessing color change in darker skin — high-yield and often taught badly

Erythema, cyanosis and jaundice can be genuinely hard to see in deeply pigmented skin. Do not rely on color alone — palpate and compare.

  • Compare to the surrounding skin and the same site on the other side.
  • Inflammation may look purple, violet, darker brown or ashen rather than pink or red.
  • Palpate for the other three signs: warmth or coolness, induration (firmness), boggy/spongy texture, edema, and pain reported by the patient.
  • Use natural or bright non-fluorescent light; check sclera, conjunctiva, oral mucosa, palms/soles and nail beds for pallor, cyanosis and jaundice.
  • Stage 1 pressure injuries are under-detected in darker skin — this is a known equity gap, so lower your threshold and document what you palpate, not only what you see.
🧠 "If you can't see it, feel it." Temperature change + induration + pain over a bony prominence is a pressure injury until proven otherwise.

✅ The head-to-toe skin check — order and content

  • Timing: a full skin assessment on admission (within the first 24 hours per most facility policy), then per policy and every shift for at-risk patients.
  • Look — color, symmetry, lesions, hygiene, hair distribution, nails (clubbing, spooning, splinter hemorrhages).
  • Touch — temperature (back of your hand), moisture, texture, turgor, edema (press over a bony area, grade pitting).
  • Don't skip the hidden places: behind the ears, under breasts and skin folds, between toes, perineum, sacrum, heels, occiput, and under every medical device (tubing, oximeter probe, O₂ tubing, cast edge, cervical collar).
  • Turn the patient — you cannot assess a sacrum you never looked at.
🧠 "Fold it, lift it, flip it." Pressure injuries hide in folds, under devices and on the side you didn't turn them to.

👵 Ageing skin vs young skin — why the same injury is worse at 85

SAME SKIN, 25 YEARS vs 85 YEARS YOUNG ADULT thick epidermis · deep rete ridges · springy collagen · fat padding 85 YEARS senile purpura thin · flat junction (shears easily) · dry · fewer vessels · almost no fat
  • Flattened dermo-epidermal junction → the layers slide apart with shear; skin tears from tape and transfers.
  • Less sebum and fewer sweat glands → dry, itchy skin (xerosis) and poorer heat tolerance.
  • Fewer vessels + slower cell turnover → wounds heal more slowly and infect more easily.
  • Less fat → bony prominences are barely padded.
  • Turgor is unreliable as a hydration measure in older adults — use the sternum or forehead, and confirm with mucous membranes, intake/output and daily weights.
🧠 Old skin is tissue paper on a wire frame: use silicone/paper tape, lift-don't-drag, and pad the frame.

📏 Depth language that every later page uses

  • Superficial / epidermal — epidermis only. Heals from the basal layer, no scar. (Sunburn, erosion, Stage 1.)
  • Partial thickness — epidermis + part of the dermis. Painful (nerves exposed), moist, heals by re-epithelialising from the surviving hair follicles and glands. (Blister, Stage 2, superficial frostbite.)
  • Full thickness — through the dermis into fat or deeper. No appendages left, so it must fill in with granulation tissue from the base and edges → scar, contracture, long healing. (Stage 3–4, deep frostbite, deep burns.)

Follow the depth story: NG-044 Pressure Injuries stages exactly this cross-section; NG-080 Wound Care turns depth into a dressing choice; NG-116 Frostbite is the cold version of the same depths.

🧠 "Appendages = seeds." If the follicles and glands survive, the wound reseeds itself from the middle. If they are gone, it can only creep in from the edges.

💊 One derm drug that shows up constantly — isotretinoin

A vitamin A derivative used for severe, nodulocystic acne that failed other therapy.

  • Pregnancy is the absolute priority. It is a potent teratogen. Prescribers and patients enroll in the manufacturer's risk-management program (iPLEDGE in the US): a negative pregnancy test before starting and before refills, and two forms of contraception used together.
  • Report mood changes or suicidal thoughts immediately — psychiatric monitoring is part of the teaching.
  • No extra vitamin A supplements (additive toxicity).
  • Avoid tetracyclines concurrently — the combination is linked to raised intracranial pressure (report severe headache, visual changes, nausea/vomiting).
  • Expect dry skin, dry eyes and dry lips: lubricating drops, may not tolerate contact lenses, and strict sun protection — the skin burns easily.
  • Monitor lipids and liver enzymes; avoid alcohol.
🧠 "A" for Acne, "A" for Absolutely no pregnancy. If a question mentions isotretinoin, the answer is almost always about contraception, mood, or sun.

✅ Universal skin protection — good for every patient on every page

  • Keep it clean and dry — gentle pH-balanced cleanser, pat don't rub, moisturise while skin is still damp.
  • Manage moisture — treat incontinence promptly, use a barrier cream/film; moisture-associated damage is not a pressure injury but sets one up.
  • Never massage a reddened bony prominence — it damages already-injured microcirculation.
  • Reposition and offload, float heels, use lift sheets, minimize head-of-bed elevation to limit shear.
  • Feed the skin — adequate protein and calories, and fluids unless restricted. Track albumin/prealbumin (typical adult albumin reference band ≈ 3.5–5.0 g/dL; ranges vary by lab) as a nutrition/inflammation marker.
  • Sun protection — broad-spectrum SPF 30+, reapply every 2 h (NG-204).
🧠 Clean · Dry · Fed · Moved. Four words that prevent most of what the rest of this set treats.

🗺️ How this page connects to the rest of the set

PageWhat it adds on top of this cross-section
NG-044 — Pressure InjuriesRedraws this exact cross-section with progressively deeper loss: Stage 1 → 4, plus unstageable and deep tissue injury; risk scoring and prevention
NG-080 — Wound CareHow wounds close (primary/secondary/tertiary intention), the healing phases, dressing choice, drains, dehiscence and evisceration
NG-116 — FrostbiteThe same depths, caused by ice crystals and vasoconstriction; rewarming rules
NG-182 — DermatitisUses the lesion vocabulary above: vesicles, weeping, lichenification, flexural vs contact-shaped distribution
NG-225 — PsoriasisWhat happens when the 28-day keratinocyte escalator speeds up to a few days: silvery scaly plaques on extensor surfaces
NG-204 — Skin CancerWhat goes wrong in the basal layer (basal cell), the keratinocytes (squamous cell) and the melanocytes (melanoma)
🧠 Learn this page once and the other six stop being separate topics — they are all "which layer, how deep, and why."
⚡

QUICK RECALL

SAY IT OUT LOUD
🧬 Epidermis · Dermis · FatAvascular barrier → workshop → padding.
🛡️ SHIELDSensation · Heat · Immunity · Excretion · Layer · D vitamin.
🚨 Non-blanchable = damageBlanches = blood behaving. Doesn't = blood escaping.
📏 Appendages = seedsPartial thickness reseeds itself. Full thickness must scar in.
🎯 Cover & check — 8 rapid-fire questions
Q1: Name the epidermal strata from deep to superficial.
Basale → spinosum → granulosum → lucidum (palms/soles only) → corneum. "Baby Skin Gets Less Cracked."
Q2: Why does a shallow abrasion ooze clear fluid rather than bleed?
Because the epidermis is avascular — it has no blood vessels. Serous fluid comes from the dermal capillaries below; you only get frank bleeding once the injury enters the dermis.
Q3: A patient has a 2 cm raised, flat-topped, silvery scaly lesion on the elbow. What is the correct lesion word?
A plaque (raised, flat-topped, greater than 1 cm) with scale. Extensor surface + silvery scale points toward psoriasis.
Q4: Difference between an erosion and an ulcer?
An erosion is loss of epidermis only and heals without a scar. An ulcer extends through the epidermis into the dermis or deeper and heals with a scar.
Q5: Your patient has non-blanchable redness over the sacrum. What is it, and what is the one thing you must not do?
A Stage 1 pressure injury. Do NOT massage the area — massage damages already-compromised microcirculation. Offload the pressure, protect the skin, document, and start prevention.
Q6: Why is skin turgor a poor hydration test in an 85-year-old?
Ageing loses elastin and dermal thickness, so skin tents even when the patient is well hydrated. Test over the sternum or forehead and confirm with mucous membranes, intake/output, and daily weights.
Q7: How do you assess for early inflammation in deeply pigmented skin?
Do not rely on redness. Compare to surrounding skin and the opposite side in good light, look for purple/violet or darker/ashen change, and palpate for temperature change, induration, boggy texture and edema — plus ask about pain.
Q8: What structures make partial-thickness wounds heal faster than full-thickness wounds?
The surviving skin appendages — hair follicles and sweat/sebaceous glands — are lined with epithelial cells that spread out to resurface the wound. Full-thickness wounds have lost them, so they must granulate in from the base and edges and will scar.