A plain-language walk through the physiology you're accountable for — built straight from your lecture decks, with a drawn figure for every idea worth picturing. Each system opens with the exact instructional objectives it covers, tagged a, b, c… Look for the Key idea boxes for the one thing to remember, and the Check yourself prompts to test recall before moving on.
Blood & Hemostasis
a Compare and contrast the function of blood and its components
Think of blood as a delivery-and-defense fluid. Just over half of it is plasma — mostly water carrying proteins, electrolytes, nutrients, and wastes. The rest is cells: red cells for carrying oxygen, white cells for defense, and platelets (really cell fragments) for plugging leaks. Every job blood does falls into one of three buckets: transport, regulation, and protection.
Plasma is the medium; the cells are the workers. Red cells transport oxygen, white cells protect, platelets and plasma proteins seal leaks. Serum is just plasma after the clotting proteins have been used up.
b Describe hematocrit and hemoglobin
Hematocrit is the percentage of blood volume made of red cells (normally about 40–45%). Hemoglobin is the oxygen-carrying protein packed inside those cells (normally about 15 g per 100 mL of blood). They travel together but measure different things: hematocrit is how many cells, hemoglobin is how much carrier protein.
Each hemoglobin is built from four globin chains, and each chain cradles a heme group with one iron atom. Each iron reversibly grabs one O₂ — so one hemoglobin carries up to four oxygen molecules. Because binding is cooperative (grabbing one O₂ makes the next easier), the oxygen-loading curve is S-shaped: it loads eagerly in the lungs and lets go readily at the tissues.
Hematocrit counts the cells; hemoglobin measures the carrier inside them. Oxygen-carrying capacity depends on hemoglobin — which is why anemia (low hemoglobin) starves tissues even when the lungs work perfectly.
c Describe hematopoiesis and its stimulus and function
Every blood cell descends from one ancestor: the pluripotent hematopoietic stem cell in the bone marrow. It divides into committed lines that mature into red cells, the various white cells, and platelets (shed from giant megakaryocytes). Production is demand-driven — low tissue oxygen ramps up red-cell output; infection ramps up white cells.
The red-cell throttle is erythropoietin (EPO), a hormone from the kidney. When oxygen delivery falls, the kidney releases more EPO, the marrow makes more red cells, oxygen delivery recovers, and EPO falls again — a clean negative-feedback loop. Building red cells also needs raw materials: iron for heme, and vitamin B₁₂ and folate for the DNA of rapidly dividing precursors.
Why does someone with failing kidneys often become anemic? (Hint: who makes EPO?) And why does B₁₂ deficiency produce large, immature red cells rather than small ones?
d Describe the molecular mechanisms involved in coagulation
Stopping bleeding happens in three quick phases. First, vascular spasm: the cut vessel clamps down. Second, the platelet plug: platelets stick to exposed collagen (helped by von Willebrand factor), activate, and recruit more platelets with ADP and thromboxane A₂. Third, coagulation: a cascade of clotting factors turns liquid blood into a fibrin mesh that cements the plug.
The cascade runs on two on-ramps that merge. The extrinsic pathway fires when tissue factor from damaged tissue meets the blood — fast, in seconds. The intrinsic pathway fires when blood contacts a charged surface like collagen — slower. Both converge on factor X, which builds prothrombin activator → this makes thrombin → thrombin cleaves fibrinogen into fibrin strands, cross-linked by factor XIII. Calcium is required at multiple steps, and the liver needs vitamin K to build several of these factors.
One sentence to hold the whole cascade: tissue factor or collagen → factor X → thrombin → fibrin. Thrombin is the hinge — it converts fibrinogen to fibrin and feeds back to make more of itself, so a clot forms fast once it starts, while antithrombin and vitamin-K economics keep it in check.
| Blood's three jobs | Transport (O₂, nutrients, waste), regulation (pH, temperature), protection (immunity, clotting). |
| Hematocrit vs. hemoglobin | Hematocrit = % red cells (~40–45%). Hemoglobin = carrier protein (~15 g/dL); sets oxygen-carrying capacity. |
| Hematopoiesis | All lines from marrow stem cells; EPO (kidney) drives red cells via negative feedback; needs iron, B₁₂, folate. |
| Coagulation | Spasm → platelet plug → cascade. Extrinsic + intrinsic → factor X → thrombin → fibrin (XIII cross-links). Ca²⁺ & vitamin K required; antithrombin restrains. |
Blood & Immunology
a Compare and contrast the function of blood and its components
White cells are the body's defense force, and each type has a specialty. To reach trouble, they leave the bloodstream by diapedesis (squeezing between vessel-wall cells) and follow chemical trails by chemotaxis.
- Neutrophils — the most numerous; first responders that swarm and phagocytize bacteria, then die (that's pus).
- Monocytes → macrophages — bigger, longer-lived phagocytes that also present antigen to lymphocytes, bridging innate and adaptive defense.
- Eosinophils — target parasites and modulate allergy.
- Basophils & mast cells — release histamine and heparin, driving inflammation and immediate allergy.
- Lymphocytes (B and T) — the specific, memory-forming adaptive cells.
b Discuss interaction of the lymphatic and immune system
Capillaries constantly leak a little fluid into tissues. The lymphatic system collects that fluid and returns it to the blood — and along the way it runs it through lymph nodes, which act as checkpoints. Inside a node, macrophages and dendritic cells trap passing antigens and show them to lymphocytes, so the drainage network doubles as a surveillance network. Block the drainage and fluid backs up as edema.
The spleen does the same job for the blood, filtering out microbes and worn-out cells. And because lymphocytes recirculate endlessly — blood → tissue → lymph → back to blood — they maximize the chance of meeting the one antigen they're built to recognize.
c Discuss functions of the immune system
Defense is layered. The outer layer is innate and nonspecific: barriers (skin, mucus, stomach acid), phagocytes, and the complement system, whose proteins opsonize (tag) microbes, attract phagocytes, and even punch holes to lyse them. The inner layer is acquired and specific: B-cells become plasma cells that pump out antibodies, while cytotoxic T-cells kill virus-infected cells directly.
Antibodies don't kill on their own — they neutralize toxins, clump microbes (agglutination), and flag targets for phagocytes and complement. The payoff of the whole acquired response is memory: cells that persist so the next encounter is faster and stronger.
d Compare and contrast innate and acquired immunity
The difference is speed vs. specificity. Innate immunity is present from birth, acts within minutes, and treats all invaders the same. Acquired immunity is tailored to one antigen and improves with experience. The proof is the response curve: the first exposure is slow and modest (matching clones must be found and multiplied); the second exposure is fast and large, dominated by high-affinity IgG. That's the logic of vaccination.
Allergy is acquired immunity misfiring. On first exposure to an allergen, the body makes IgE that coats mast cells. On the next exposure, the allergen cross-links that IgE, mast cells degranulate, and histamine floods out — vasodilation, leaky vessels, swelling, itch.
Innate = fast and generic; acquired = specific and remembered. Antibodies tag and clump rather than kill. Allergy is the acquired system aiming its IgE-and-histamine machinery at a harmless target.
| White cells | Neutrophils (first responders), macrophages (eat + present), eosinophils (parasites), basophils/mast (histamine), lymphocytes (specific + memory). Exit via diapedesis, home in by chemotaxis. |
| Lymphatic ↔ immune | Lymphatics return leaked fluid and filter it through nodes (antigen checkpoints); spleen filters blood; lymphocytes recirculate. Blocked drainage → edema. |
| Immune functions | Innate: barriers, phagocytes, complement (tag/recruit/lyse). Acquired: antibodies (neutralize, agglutinate, opsonize) and cytotoxic T-cells; memory persists. |
| Innate vs. acquired + allergy | Innate = fast/general; acquired = specific/remembered (2nd response bigger). Allergy = IgE-coated mast cells releasing histamine on re-exposure. |
Gastrointestinal Physiology
a Describe the physiology of GI motility, gastric secretion, and gastric hormones
The gut has its own nervous system — the enteric nervous system — that can run motility and secretion on its own, with the autonomic nerves only turning the dial. The underlying rhythm comes from slow waves set by pacemaker cells. Two movement patterns matter: peristalsis pushes contents forward, while segmentation chops and mixes them in place.
Gastric secretion switches on in three phases: cephalic (sight/smell/thought of food, via the vagus — before food even arrives), gastric (stomach stretch and protein trigger local reflexes and gastrin), and intestinal (chyme in the duodenum fine-tunes the rest). Three hormones run the show: gastrin (stomach — raises acid and motility), secretin (duodenum senses acid — calls for pancreatic bicarbonate), and cholecystokinin/CCK (duodenum senses fat/protein — contracts the gallbladder, releases pancreatic enzymes, slows emptying).
b Describe digestive enzymes of the GI tract
Digestion is a relay handed down the tract. Carbohydrate starts in the mouth (salivary amylase), pauses in the acidic stomach, and finishes in the small intestine (pancreatic amylase → brush-border disaccharidases like lactase). Protein starts in the stomach (pepsin, which needs acid) and finishes with pancreatic proteases and brush-border peptidases. Fat is barely touched until the small intestine, where bile emulsifies it and pancreatic lipase does the work.
c & d Describe the function of the biliary system; describe the exocrine function of the pancreas
These two empty into the same place (the duodenum) and are worth learning together. The liver continuously makes bile; between meals the gallbladder stores and concentrates it. When fat arrives, CCK squeezes the gallbladder and bile flows in. Bile salts are amphipathic — one end likes water, one likes fat — so they emulsify fat into tiny droplets that lipase can attack. Most bile salts are then reabsorbed in the ileum and recycled (enterohepatic circulation).
The exocrine pancreas supplies the two things the duodenum needs: bicarbonate (on secretin's order) to neutralize stomach acid, and digestive enzymes (on CCK's order) for all three food groups.
e Describe the functions of the liver
Everything absorbed from the gut drains first through the liver via the portal vein before reaching the rest of the body — so the liver gets first pass at every nutrient and toxin. Its jobs: buffer blood glucose (store as glycogen after meals, release between them), detoxify drugs and toxins, convert toxic ammonia into urea, make bile and most plasma proteins, store iron and vitamins, and filter blood with resident macrophages (Kupffer cells).
f Describe protein, carbohydrates, and lipid absorption
The small intestine is folded into villi and microvilli to maximize surface area. Glucose and amino acids are pulled into the cell by sodium-coupled transport — the sodium gradient (kept up by the Na⁺/K⁺ pump) drags them in, then they pass to the blood and head to the liver via the portal vein. Fat is different: broken-down fats ride bile-salt micelles to the cell, are repackaged into chylomicrons, and — being too big for blood capillaries — enter the lymph first, joining the bloodstream later.
g Explain the process of defecation
A meal entering the stomach triggers the gastrocolic reflex, driving mass movements that push stool into the rectum. Rectal stretch reflexively relaxes the internal anal sphincter (smooth muscle, involuntary) — but the external anal sphincter is skeletal muscle under conscious control, which is why defecation can be voluntarily delayed until it's convenient.
Two sphincters, two kinds of control: the inner one opens on its own by reflex; the outer one is yours to hold. That split is the whole trick of voluntary continence.
| Motility & hormones | Enteric NS + slow waves. Peristalsis pushes, segmentation mixes. Gastrin (acid+motility), secretin (bicarbonate for acid), CCK (bile+enzymes for fat). |
| Enzymes | Carbs: amylase → disaccharidases. Protein: pepsin (acid) → proteases/peptidases. Fat: bile + lipase. Proteases secreted as zymogens. |
| Bile & pancreas | Liver makes bile; gallbladder stores/concentrates; CCK releases it; amphipathic bile salts emulsify fat; recycled in ileum. Pancreas: bicarbonate (secretin) + enzymes (CCK). |
| Liver | First-pass via portal vein: glucose buffer, detox, urea, bile, plasma proteins, storage, Kupffer filtering. |
| Absorption | Villi/microvilli surface. Sugars & amino acids: Na⁺-coupled → blood → liver. Fat: micelles → chylomicrons → lymph → blood. |
| Defecation | Gastrocolic reflex → mass movement. Internal sphincter (involuntary) relaxes; external sphincter (voluntary) allows delay. |
Metabolism & the Liver
a Review the functions of the liver
You met the liver in the GI unit; here it's the metabolic manager. Its headline jobs: buffer blood glucose (store glycogen after meals, release glucose between them), detoxify drugs and convert ammonia to urea, make bile for fat digestion, build plasma proteins (albumin, clotting factors), and store iron and vitamins. Because portal blood reaches it first, it processes nutrients before the rest of the body sees them.
b Describe the production, transport, and conversion of glucose
Burning glucose for ATP runs in stages. Glycolysis (in the cytoplasm, no oxygen needed) nets just 2 ATP and yields pyruvate. Pyruvate feeds the citric acid cycle, and the electron carriers it produces drive oxidative phosphorylation — where the vast majority of ATP is made, using oxygen. So: a little energy fast without oxygen, a lot of energy with it.
Blood glucose is held steady by two opposing hormones: insulin lowers it (drives uptake and storage after meals), glucagon raises it (breaks down glycogen and makes new glucose between meals). When glycogen runs low, the liver builds glucose from scratch — gluconeogenesis — because the brain runs almost entirely on glucose.
c Describe the production, transport, and conversion of lipids
Fat is the body's densest fuel (~9 kcal/g, stored nearly water-free). To burn it, beta-oxidation chops fatty acids into two-carbon acetyl-CoA units that feed the citric acid cycle. During fasting, the liver turns surplus acetyl-CoA into ketone bodies — an alternative fuel the brain can use, sparing protein.
Because fat doesn't dissolve in blood, it travels inside lipoproteins, each with a job: chylomicrons carry dietary fat from the gut, VLDL carries liver-made fat out to tissues, LDL delivers cholesterol to tissues, and HDL brings excess cholesterol back to the liver (the "good" reverse route).
d Describe the production, transport, and conversion of protein
Amino acids sit in a constantly refreshed pool, drawn on to build proteins and topped up by diet and protein turnover. To burn an amino acid for energy, its nitrogen must first be removed by deamination or transamination; the leftover carbon skeleton feeds energy pathways. The freed nitrogen becomes toxic ammonia, which the liver's urea cycle converts to urea for the kidneys to excrete. Body protein is a last-resort fuel — spared until carbohydrate and fat run low. Hormones tip the balance: growth hormone builds protein (positive nitrogen balance); cortisol breaks it down for gluconeogenesis.
Glucose is fast fuel (little without oxygen, lots with it); fat is the dense reserve with its own delivery fleet; protein is spared for fuel and its nitrogen must be detoxified into urea. The liver quietly coordinates all three.
| Liver functions | Glucose buffer, detox + urea, bile, plasma proteins, storage; first-pass via portal vein. |
| Glucose | Glycolysis (2 ATP, no O₂) → citric acid cycle → oxidative phosphorylation (most ATP, needs O₂). Insulin lowers, glucagon raises; gluconeogenesis feeds the glucose-dependent brain. |
| Lipids | Beta-oxidation → acetyl-CoA; fasting → ketones. Transport: chylomicrons (diet), VLDL (liver out), LDL (to tissues), HDL (back to liver). |
| Protein | Amino-acid pool; deamination/transamination frees the skeleton; urea cycle disposes nitrogen. Last-resort fuel. GH anabolic, cortisol catabolic. |
Nutrition, Energetics & Thermoregulation
a Discuss body energy balance
Body weight is an accounting problem: energy in (food) versus energy out (basal metabolism + activity + the cost of digesting food). A surplus is stored, mostly as fat; a deficit draws stores down. The fuels aren't equal: carbohydrate and protein give about 4 kcal/g, fat about 9. That's why fat is the biggest reserve (dense, nearly water-free), glycogen is a small quick-access store, and free glucose is only minutes' worth.
In starvation the body burns fuels in order: glycogen first (gone within a day), then increasingly fat, with body protein spared until late. Appetite is set in the hypothalamus — a feeding center and a satiety center — nudged by hormones like ghrelin (hunger) and leptin (fullness/fat stores).
b Analyze body temperature and how it is controlled
The hypothalamus is the thermostat, holding core temperature near 37 °C by balancing heat made against heat lost. When cold, it conserves and makes heat: skin vasoconstriction and shivering. When hot, it dumps heat: skin vasodilation and sweating — and sweat only cools when it evaporates. Heat leaves the body four ways: radiation, conduction, convection, and evaporation.
Fever isn't broken control — it's the thermostat reset higher. Pyrogens raise the set point, so the body feels cold and makes heat (chills, shivering) until it reaches the new, higher target. When the fever "breaks," the set point drops back and the now-too-warm body flushes and sweats to shed the excess.
c Discuss metabolic rate
Basal metabolic rate (BMR) is the energy to keep the resting body running, measured under strict conditions (rested, fasting, comfortable temperature) so nothing inflates it. In a typical day it's the largest slice of energy use. On top of it sit physical activity (the most variable slice) and the thermic effect of food — the cost of digesting a meal, which is high for protein.
What moves the rate? Thyroid hormone and sympathetic activity push it up; larger body size means a larger total; and it tends to fall with age as lean muscle is lost. A neat bonus: the respiratory quotient (CO₂ out ÷ O₂ used) reveals the fuel — about 1.0 for carbohydrate, 0.7 for fat.
Weight is energy in vs. out; temperature is heat made vs. lost around a hypothalamic set point; metabolic rate is mostly the resting cost of being alive, dialed by thyroid, sympathetic tone, body size, and age.
| Energy balance | In vs. out; surplus stored as fat. Carbs/protein 4 kcal/g, fat 9. Stores: fat (huge) > glycogen (~1 day) > glucose (minutes). Starvation: glycogen → fat → protein. Hypothalamus + ghrelin/leptin set appetite. |
| Temperature | Hypothalamic set point ≈ 37 °C. Cold: vasoconstrict + shiver. Hot: vasodilate + sweat (evaporation cools). Loss: radiation, conduction, convection, evaporation. Fever = raised set point. |
| Metabolic rate | BMR = largest slice (measured rested/fasting). + activity + thermic effect of food. ↑ thyroid, sympathetic, body size; ↓ with age. RQ: 1.0 carb, 0.7 fat. |
Respiration I — Ventilation & Gas Exchange
a & b Compare and contrast the functions of the muscles of respiration; explain compliance and elasticity of lung
Quiet breathing is mostly the diaphragm (driven by the phrenic nerve from the neck). It contracts and drops, the chest enlarges, and by Boyle's law a bigger space means lower pressure — so air flows in. Heavy breathing recruits accessory muscles (neck muscles to inhale harder; abdominals and internal intercostals to force air out).
The lungs stay inflated because of the intrapleural pressure — the slightly negative pressure in the thin space between lung and chest wall. The lung's natural elastic recoil wants to collapse it inward; that negative pressure holds it open. Compliance is how easily the lung inflates. If air breaches the pleural space (pneumothorax), the negative pressure is lost and the lung recoils shut.
c Compare and contrast lung capacities and lung volumes
Four volumes add up to describe the lungs. Tidal volume is a normal breath. Inspiratory and expiratory reserve are the extra you can pull in or push out. Residual volume is what always stays — it can never be exhaled, which is why spirometry (which measures moved air) can't capture it. Capacities are just volumes added together: vital capacity (all you can move) and total lung capacity (everything, including residual).
d Describe the function of surfactant
The watery lining of an alveolus creates surface tension that tries to collapse it — and by the law of Laplace, smaller alveoli generate stronger collapsing pressure, so they'd empty into bigger ones. Surfactant (a phospholipid made by alveolar cells) slips between the water molecules and lowers that tension — more so in small alveoli. The result: alveoli stay stable and open, and the lung is far easier to inflate. Without it (as in premature infants), alveoli collapse and every breath is a struggle.
e & f Explain gas exchange taking place in the lungs; review the respiratory membrane
Gases move by diffusion down partial-pressure gradients — no pumping. In the lung, alveolar oxygen is high and the arriving blood's is low, so O₂ flows into blood; CO₂ is higher in blood, so it flows out. Exchange is fast and complete with a safety margin — blood is fully loaded well before it leaves the capillary.
It's fast because the respiratory membrane is built for it: an enormous total surface area and an incredibly thin barrier (~0.2–0.6 µm). Diffusion speeds up with more area, a thinner membrane, a steeper gradient, and higher gas solubility — which is why CO₂ (very soluble) crosses easily despite a smaller gradient. Thicken the membrane with fluid and exchange slows.
Breathing is a pressure trick (Boyle's law) with the lung held open by a pleural vacuum; surfactant keeps the small sacs from collapsing; and gas exchange is pure diffusion across a huge, paper-thin membrane.
| Muscles | Diaphragm (phrenic nerve) for quiet breathing; accessory muscles for forced. Contract → volume ↑ → pressure ↓ → air in (Boyle's law). |
| Compliance/elasticity | Compliance = ease of inflation; elastic recoil pulls inward; negative intrapleural pressure holds lungs open; pneumothorax → collapse. |
| Volumes/capacities | Tidal + IRV + ERV + residual. Residual can't be exhaled (spirometry misses it). VC = movable air; TLC = everything. |
| Surfactant | Lowers surface tension (most in small alveoli) → raises compliance, prevents collapse (Laplace). |
| Gas exchange / membrane | Diffusion down partial-pressure gradients; O₂ in, CO₂ out; complete with safety margin. Fast because area is huge and membrane thin; CO₂ crosses easily (soluble). |
Respiration II — Gas Transport & Control
a Compare and contrast the respiratory centers of the brain
The basic rhythm is generated in the medulla; the pons (pneumotaxic center) smooths and fine-tunes it. The strongest minute-to-minute driver isn't oxygen — it's carbon dioxide. Central chemoreceptors in the medulla sense the H⁺ produced when CO₂ rises and push ventilation up. Peripheral chemoreceptors (carotid and aortic bodies) mainly back up the system by sensing dangerously low oxygen. A stretch reflex (Hering-Breuer) guards against over-inflation.
b & e Describe oxygen transport within the cardiopulmonary circulation; describe gas exchange at the tissue level
Oxygen barely dissolves in plasma, so ~98% rides on hemoglobin. The O₂–hemoglobin curve is S-shaped: its flat top means blood leaves the lungs nearly full even if lung oxygen dips; its steep middle means small drops in tissue oxygen release a lot. Working tissues shift the curve right — with more CO₂, acid, heat, and BPG — which lowers hemoglobin's grip and dumps more oxygen exactly where demand is highest. A left shift (cold, low CO₂, fetal hemoglobin, carbon monoxide) makes hemoglobin hold on tighter.
c Describe carbon dioxide transport within the cardiopulmonary circulation
CO₂ travels three ways: most as bicarbonate (~70%), some bound to hemoglobin as carbamino compounds (~20%, on the globin, not the iron), and a little dissolved. The key enzyme is carbonic anhydrase inside red cells, which rapidly turns CO₂ + water into carbonic acid → bicarbonate + H⁺. As bicarbonate leaves the cell, chloride shifts in to keep the charge balanced (the "chloride shift"). At the lungs, every step runs in reverse and CO₂ is breathed out.
d Describe respiratory influence on pH
That bicarbonate chemistry is the bridge to acid-base balance: CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻. Because the lungs control CO₂, breathing directly moves pH. Hyperventilation blows off CO₂, pulling the reaction left, dropping H⁺ → alkalosis (higher pH). Hypoventilation traps CO₂, pushing right, raising H⁺ → acidosis (lower pH). The lungs adjust within minutes (fast but limited); the kidneys handle bicarbonate over hours-to-days (slow but thorough).
CO₂ runs the show: it's the main drive to breathe, the main form of carbon-dioxide transport (as bicarbonate), and — because it's a hidden acid — the fast lever the lungs use to control blood pH. Oxygen, meanwhile, rides on hemoglobin and is unloaded right where work is hardest.
| Control centers | Medulla makes the rhythm; pons refines it. Central chemoreceptors sense CO₂/H⁺ (main driver); peripheral sense low O₂ (backup). Hering-Breuer guards over-inflation. |
| O₂ transport | ~98% on hemoglobin. S-curve: flat top loads in lungs, steep middle unloads at tissues. Right shift (CO₂, acid, heat, BPG) unloads more; left shift (cold, CO, fetal Hb) holds tighter. |
| CO₂ transport | ~70% bicarbonate (carbonic anhydrase), ~23% carbamino-Hb, ~7% dissolved. Chloride shift maintains charge. |
| Breathing & pH | CO₂ + H₂O ⇌ H⁺ + HCO₃⁻. Hyperventilation → alkalosis; hypoventilation → acidosis. Lungs fast, kidneys slow/thorough. |
| Tissue exchange | Low tissue PO₂ → O₂ diffuses out; high tissue PCO₂ → CO₂ diffuses in; right-shifted curve boosts unloading in active tissue. |