Your BIO 262 course, written out as study material instead of a file list. Each week opens with the one idea that makes the rest make sense, then the mechanism, then a comparison table and the traps. Open only the week you are revising.
A T cell is a lymphocyte that got an education. It is born in bone marrow like every other blood cell, but it does not become useful until it passes through the thymus — which is what the T stands for.
Vessels follow one rule too: the thicker the muscle layer, the closer to the heart's pressure.
Roughly 98% of them fail and are destroyed.
That brutal filter is what stops your immune system attacking you.
When negative selection fails, self-attacking T cells escape — that is the root of autoimmune disease (type 1 diabetes, MS, rheumatoid arthritis).
DiGeorge syndrome = no thymus = no working T cells.
| CD4 — Helper | CD8 — Cytotoxic | |
|---|---|---|
| Job | Directs everyone else; releases cytokines | Kills infected cells directly |
| Binds | MHC class II | MHC class I |
| Memory hook | 4 = 2 × 2 (class II) | 8 = 1 × 8 (class I) |
| Lost in HIV | Yes — this is the cell HIV destroys | Preserved early on |
A normal CD4 count is roughly 500–1500. AIDS is defined at CD4 < 200,
which is when opportunistic infections take hold. That single number shows up constantly.
| Layer | What it is | Why you care |
|---|---|---|
| Tunica intima | Endothelium, one cell thick | Damage here starts atherosclerosis and clots |
| Tunica media | Smooth muscle + elastic fibers | Constricts and dilates → controls blood pressure |
| Tunica externa | Collagen, anchors the vessel | Holds shape, carries its own blood supply |
Arteries have a thick tunica media because they take the ventricle's pressure head-on. They stay round when empty.
Veins have a thin media, a wide lumen, and valves. They collapse when empty and hold about 65% of your total blood volume at any moment — they are the reservoir.
Capillaries are endothelium only. One cell thick is the whole point: that is the only place exchange happens.
“Arteries carry oxygenated blood” is false. The pulmonary artery carries deoxygenated blood to the lungs; the pulmonary veins carry oxygenated blood back.
Arteries carry blood away from the heart. That is the actual definition.
There are only four tissue types in the entire body. Every organ is a combination of them. Learn the four and you can reason about any organ you meet.
| Tissue | One-line job | Where | Repairs? |
|---|---|---|---|
| Epithelial | Covers, lines, secretes | Skin surface, gut lining, glands | Excellent — divides fast |
| Connective | Binds and supports | Bone, blood, fat, tendon, cartilage | Varies — cartilage barely heals |
| Muscle | Contracts | Skeletal, cardiac, smooth | Poor — scars instead |
| Nervous | Conducts signals | Brain, cord, nerves | Almost none in CNS |
Tissue that touches the outside world regenerates. Tissue that does the thinking does not. That is why a skin graze vanishes in a week and a spinal cord injury is permanent.
It is the only type defined by its matrix rather than its cells — the non-living material the cells sit in. Change the matrix and you change the tissue completely:
| Layer | Made of | Key point |
|---|---|---|
| Epidermis | Stratified squamous epithelium | No blood supply. Fed by diffusion from below |
| Dermis | Connective tissue | Vessels, nerves, follicles, glands — where pain is felt |
| Hypodermis | Fat (subcutaneous) | Insulation, cushioning, where SubQ injections go |
Superficial — epidermis only. Red, dry, painful. Heals itself.
Partial thickness — into dermis. Blisters, and the most painful, because dermal nerve endings are exposed but alive.
Full thickness destroys the nerves — so it is painless. Painless is worse, not better.
Asked which burn hurts most, the answer is partial thickness, not full thickness. Students lose this mark constantly by assuming deeper always means more pain.
Bone is not scaffolding. It is an organ that is rebuilt continuously — and it is where your body stores about 99% of its calcium.
When blood calcium falls, the skeleton is spent to fix it. Bone strength is always the lower priority.
| Cell | Does | Memory hook |
|---|---|---|
| Osteoblast | Builds new bone matrix | B = Build |
| Osteoclast | Chews bone, releasing calcium to blood | C = Crush |
| Osteocyte | Mature cell; senses strain, directs the other two | The retired supervisor |
Two hormones pull in opposite directions, and they are constantly confused on exams:
| PTH (parathyroid) | Calcitonin (thyroid) | |
|---|---|---|
| Released when | Blood calcium is LOW | Blood calcium is HIGH |
| Acts on bone | Activates osteoclasts → breaks bone down | Inhibits osteoclasts |
| Kidney | Reabsorbs calcium, activates vitamin D | Excretes calcium |
| Net effect | Blood calcium ↑ | Blood calcium ↓ |
“Stones, bones, abdominal groans, and psychiatric moans.” That is hypercalcemia: kidney stones, bone pain, constipation and ileus, confusion and depression.
Flip every sign for hypocalcemia — instead of sluggish, everything becomes twitchy: tetany, spasm, tingling, positive Chvostek and Trousseau signs.
Estrogen restrains osteoclasts. When estrogen drops, that brake is released, resorption outpaces building, and bone density falls.
Same logic explains steroid-induced osteoporosis: corticosteroids suppress osteoblasts, so building slows while chewing continues.
Muscle contraction is a calcium story. Every step exists to get calcium into the muscle cell, and relaxation is simply pumping it back out again.
The filaments never shorten. Actin and myosin slide past each other, so the sarcomere shortens while the proteins stay the same length.
Calcium's actual job: it moves troponin and tropomyosin off the actin binding sites. Those sites are blocked at rest — calcium unlocks the door, it does not push.
ATP powers contraction — but it is also required to release myosin from actin.
No ATP means the bridges cannot let go. That is rigor mortis.
| Phase | Ion moving | Membrane |
|---|---|---|
| Resting | Na⁺/K⁺ pump holds the gradient | −70 mV inside negative |
| Depolarization | Na⁺ rushes IN | Shoots toward +30 mV |
| Repolarization | K⁺ flows OUT | Falls back toward rest |
| Refractory | Pump resets gradients | Cannot fire again yet |
Resting potential is the potassium gradient. Change serum K⁺ and you change whether every nerve and muscle in the body — including the heart — can fire correctly.
That is why potassium is the electrolyte that kills fastest, and why it is never given IV push.
Myelin insulates the axon so the signal jumps node to node (saltatory conduction) instead of crawling. Strip the myelin — as in multiple sclerosis — and conduction slows or fails. That is the whole disease in one sentence.
Both organs are transducers. The eye converts light into electricity; the ear converts vibration into electricity. Everything else is plumbing that protects and focuses.
| Rods | Cones | |
|---|---|---|
| Detect | Dim light, movement | Color, sharp detail |
| Where | Peripheral retina | Concentrated at the fovea |
| Memory hook | Rods = niGHt | Cones = Color |
Aqueous humor cannot drain → pressure rises → the optic nerve is compressed.
Because rods sit in the periphery, peripheral vision goes first and central vision stays normal for years — so it is painless and unnoticed until late.
Acute angle-closure glaucoma is the exception: sudden severe eye pain, halos, a fixed pupil. That is an emergency.
The semicircular canals sit next to the cochlea and sense head rotation. That shared address is why ear infections and Ménière's disease cause vertigo — not just hearing loss.
Conductive — sound cannot get in. Wax, fluid, a perforated drum, otosclerosis. Often fixable.
Sensorineural — the hair cells or nerve are damaged. Noise, ageing, ototoxic drugs. Usually permanent.
Ototoxic offenders worth knowing: aminoglycosides (gentamicin), loop diuretics, high-dose aspirin, cisplatin.
A hormone only affects a cell that has its receptor. The bloodstream carries it everywhere; the receptor decides who listens. That single fact explains why one hormone can do several unrelated things in different tissues.
The output shuts off its own trigger, like a thermostat: Hypothalamus → pituitary → gland → hormone → signals back to switch the hypothalamus off.
Understand this loop and you can predict every lab pattern in endocrinology instead of memorizing them.
Compare the gland hormone with its stimulating hormone:
Both hormones moving the same direction = the problem is upstream, in the pituitary.
| Steroid (lipid-soluble) | Peptide (water-soluble) | |
|---|---|---|
| Examples | Cortisol, aldosterone, estrogen, testosterone | Insulin, ADH, growth hormone |
| Receptor sits | Inside the cell | On the cell surface |
| Acts by | Switching genes on → makes new protein | Second messengers → activates existing protein |
| Speed | Slow (hours) but long-lasting | Fast (seconds) but brief |
Long-term steroid dosing convinces the hypothalamus there is plenty of cortisol, so it stops signaling and the adrenal glands atrophy.
Stop suddenly and there is no cortisol from anywhere — adrenal crisis. Steroids are always tapered.
| ADH (vasopressin) | Aldosterone | |
|---|---|---|
| From | Posterior pituitary | Adrenal cortex |
| Retains | Water only | Sodium (water follows) |
| Effect on Na⁺ | Dilutes it — sodium falls | Raises sodium |
| Too much | SIADH — concentrated urine, low serum Na⁺ | Conn's — hypertension, low K⁺ |
| Too little | Diabetes insipidus — liters of dilute urine | Addison's — low Na⁺, high K⁺ |
“SIADH soaks. DI drains.” SIADH holds water in and dilutes the blood. Diabetes insipidus pours it out and concentrates the blood.
Clotting is a controlled emergency. The body must plug a hole fast enough to stop blood loss, but not so eagerly that it blocks a healthy vessel. Nearly every bleeding or clotting disorder is that balance tipping one way.
| Component | Share | Job |
|---|---|---|
| Plasma | ~55% | Water, albumin, clotting factors, electrolytes |
| RBCs | ~45% | Carry O₂ on hemoglobin. No nucleus, live ~120 days |
| WBCs + platelets | <1% | Defense and clotting |
Ditching the nucleus frees space for more hemoglobin and lets the cell bend through capillaries narrower than itself. The cost: it cannot repair itself or divide, which is why it only lasts 120 days.
You do not need every factor. You need which test watches which pathway, because that is what drug monitoring depends on:
| Intrinsic | Extrinsic | |
|---|---|---|
| Triggered by | Damage inside the vessel | Tissue injury outside the vessel |
| Measured by | aPTT | PT / INR |
| Drug monitored | Heparin | Warfarin |
| Antidote | Protamine sulfate | Vitamin K |
“PT / WEPT” — PT goes with Warfarin, Extrinsic.
Everything left over — aPTT — goes with heparin and intrinsic.
Warfarin blocks vitamin-K-dependent factors, which is exactly why vitamin K reverses it. The antidote is the mechanism run backwards.
Three conditions, and a DVT usually needs more than one:
A post-op patient on bed rest has all three at once.
One equation runs all of cardiology:
CO = HR × SV
Cardiac output is heart rate times stroke volume. Every cardiac drug and every cardiac disease works by changing one of those two numbers.
| Dial | Plain English | Raised by | Lowered by |
|---|---|---|---|
| Preload | How full the ventricle is before it squeezes | IV fluids, heart failure | Diuretics, bleeding, nitrates |
| Afterload | The resistance it must squeeze against | Hypertension, vasoconstriction | ACE inhibitors, vasodilators |
| Contractility | How hard the muscle squeezes | Digoxin, dobutamine, epinephrine | Beta blockers, ischemia, acidosis |
Stretch a healthy ventricle more and it squeezes harder — like a rubber band. More preload gives more stroke volume.
But only up to a point. Overstretch it and force falls off, because the actin and myosin filaments no longer overlap properly.
That drop-off is decompensated heart failure. It is why fluid overload makes a failing heart worse, not better.
EF is the percentage of ventricular volume ejected per beat. Normal is
55–70%. A healthy heart never empties completely.
The AV delay is deliberate. Without it the atria and ventricles would contract together and nothing would move forward.
Ventricles contract from the apex up, squeezing blood toward the outflow valves — like squeezing a tube of toothpaste from the bottom.
If the SA node fails, the AV node takes over at ~40–60, and the Purkinje system at ~20–40. The further down the back-up, the slower and less reliable it is.
You have a fast, dumb system and a slow, clever one. Innate immunity responds in minutes to anything foreign. Adaptive immunity takes days but remembers forever.
| Innate | Adaptive | |
|---|---|---|
| Speed | Minutes to hours | Days on first exposure |
| Specific? | No — same response to everything | Yes — targeted to one antigen |
| Memory? | None | Yes — the basis of vaccination |
| Players | Skin, mucus, neutrophils, macrophages, fever, complement | B cells (antibodies), T cells |
The four classic signs are all one process: vessels dilate and leak on purpose.
It is not the infection. It is your response to it.
Active — you make the antibodies. Slow to build, long-lasting. Infection, or a vaccine.
Passive — antibodies are given to you. Instant, but temporary. Placental transfer, breast milk, immunoglobulin injections.
Instant protection is always temporary. Lasting protection always takes time to build.
The hypothalamic set point is deliberately raised — most pathogens replicate poorly at higher temperatures and immune enzymes work faster.
Which is why shivering comes first: your body is generating heat to reach the new set point. Chills mean the fever is still climbing.
Breathing is two separate jobs. Ventilation moves air in and out. Respiration is the gas actually crossing into blood. A patient can ventilate beautifully and still not oxygenate.
Only pressure gradients. The diaphragm contracts and flattens → the chest volume rises → pressure inside drops below atmospheric → air is pushed in.
Quiet exhalation is passive — the lung's own elastic recoil. It costs no energy.
Surfactant reduces surface tension so alveoli do not collapse on themselves at the end of each breath.
It is not produced in adequate amounts until roughly week 34–36 of gestation — which is precisely why preterm infants develop respiratory distress syndrome, and why mothers in preterm labor are given steroids to accelerate its production.
| Shift | Means | Caused by |
|---|---|---|
| RIGHT | Hemoglobin releases O₂ more easily — tissues get more | Acid, ↑CO₂, fever, exercise |
| LEFT | Hemoglobin holds O₂ tightly — tissues get less | Alkalosis, ↓CO₂, hypothermia |
“Right = Release.” Both start with R.
And it makes physiological sense: a hot, acidic, hard-working muscle needs oxygen — so those exact conditions make hemoglobin let go of it.
Take them in this order and you cannot get lost:
7.35–7.45 — below is acidosis, above is alkalosis35–45 — the lung number. Moves opposite to pH when respiratory22–26 — the kidney number. Moves with pH when metabolicWhichever value matches the pH direction is the culprit.
In chronic CO₂ retention the kidneys compensate by holding bicarbonate, so pH sits near normal with a high CO₂ and a high HCO₃⁻. That is compensated respiratory acidosis, not a normal gas.
A "normal" pH with two abnormal values is compensation, never health.
Sources. Written from OpenStax Anatomy & Physiology 2e, which is free and openly licensed (CC BY 4.0), and from standard nursing physiology. Nothing here is copied from a publisher's material, and no file on this page opens anyone's private Drive.
For deeper reading, your own references: Color Atlas of Pathophysiology (Silbernagl & Lang), Pathophysiology for Nurses at a Glance (Nair), and WTCS Nursing Pharmacology 2e.