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Physiology Field Guide

PAJ 5000 Graduate Physiology · Class of 2028

Blood & Hemostasis · Blood & Immunology · GI Physiology · Metabolism & the Liver · Nutrition, Energetics & Thermoregulation · Respiration I & II

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.

System 01 — Chapter 37

Blood & Hemostasis

Red cells & hemoglobin · blood formation · the clotting cascade
You'll be able to…
a Compare and contrast the function of blood and its components.
b Describe hematocrit and hemoglobin.
c Describe hematopoiesis and its stimulus and function.
d Describe the molecular mechanisms involved in coagulation.

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 — ~55% water + proteins (albumin, antibodies, clotting factors), electrolytes, nutrients Buffy coat — <1% white cells + platelets Red cells — ~45% this packed fraction is the hematocrit Three jobs: transport · regulation · protection
Figure 1 · A spun tube of blood Spin blood in a tube and it settles by weight: pale plasma on top, a thin white "buffy coat" of white cells and platelets in the middle, and heavy red cells at the bottom. The red-cell fraction is the hematocrit — the single number that tells you how much oxygen-carrying tissue is in the blood.
Key idea

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.

4 globin chains · 4 heme irons · 4 O₂ oxygen level (PO₂) → % saturated → steep middle = easy unloading flat top = full in the lungs
Figure 2 · Hemoglobin and its S-shaped curve Four iron sites per molecule, each holding one O₂. Cooperative binding gives the curve its S shape: the flat top means blood leaves the lungs nearly full even if lung oxygen dips a little, and the steep middle means small drops in tissue oxygen unload a lot of it right where it's needed.
Key idea

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.

stem cell (marrow) red cells (O₂) white cells (defense) platelets (clotting) ↓ tissue O₂ kidney releasesEPO marrow → more RBCs O₂ deliveryrecovers turns EPO back down
Figure 3 · One ancestor, three products — and the EPO thermostat Left: the marrow stem cell branches into red cells, white cells, and platelets. Right: erythropoietin works like a thermostat for red-cell mass — low oxygen turns it up, restored oxygen turns it back down.
Check yourself

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.

EXTRINSIC tissue factor · fast (sec) INTRINSIC contact w/ collagen · slower Factor X → Xa common pathway prothrombin activator thrombin needs Ca²⁺ needs Ca²⁺ fibrinogen → fibrin mesh (cross-linked by factor XIII) Two brakes & a supply line • Antithrombin III inactivates thrombin (heparin speeds it) • Smooth endothelium repels platelets · Vitamin K builds factors in the liver
Figure 4 · Two on-ramps, one highway The extrinsic pathway (tissue damage) is the fast starter; the intrinsic pathway (blood contacting collagen) is the slower one. Both merge at factor X and run down the same spine to thrombin and fibrin. Notice the built-in brakes — antithrombin and healthy endothelium — that keep the clot from spreading.
Key idea

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 & Hemostasis — one-glance recap
Blood's three jobsTransport (O₂, nutrients, waste), regulation (pH, temperature), protection (immunity, clotting).
Hematocrit vs. hemoglobinHematocrit = % red cells (~40–45%). Hemoglobin = carrier protein (~15 g/dL); sets oxygen-carrying capacity.
HematopoiesisAll lines from marrow stem cells; EPO (kidney) drives red cells via negative feedback; needs iron, B₁₂, folate.
CoagulationSpasm → platelet plug → cascade. Extrinsic + intrinsic → factor X → thrombin → fibrin (XIII cross-links). Ca²⁺ & vitamin K required; antithrombin restrains.
System 02 — Chapters 34–35

Blood & Immunology

White cells · the lymphatic partnership · immune defense · allergy
You'll be able to…
a Compare and contrast the function of blood and its components.
b Discuss interaction of the lymphatic and immune system.
c Discuss functions of the immune system.
d Compare and contrast innate and acquired immunity.

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.
Neutrophilfirst responder Macrophageeat + present Eosinophilparasites Basophil/Masthistamine Lymphocytespecific + memory capillary wall diapedesis (slips through the wall), then follows the trail — chemotaxis
Figure 5 · Five specialists, one goal Neutrophils and macrophages do the eating; eosinophils handle parasites; basophils/mast cells fire the inflammation alarm; lymphocytes bring specificity and memory. To get to the fight, a white cell slips through the vessel wall and homes in on chemical signals.

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.

capillary leak tissue fluid lymph node checkpoint: traps & presents antigen back to blood Backed-up drainage = edema · The spleen filters the blood the same way.
Figure 6 · The drain that also stands guard Lymphatics reclaim leaked fluid and route it through nodes, where antigens are caught and shown to lymphocytes. Fluid balance and immune surveillance are the same plumbing.

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.

Innate (fast, general) barriers: skin, mucus, acid phagocytes eat invaders complement: tag · recruit · lyse Acquired (specific, memory) B → plasma cells → antibodies cytotoxic T kills infected cells helper T coordinates all of it memory cells remain Antibodies… • neutralize toxins • agglutinate (clump) • opsonize (flag for eating) • activate complement two arms bound: Y-shape
Figure 7 · Two layers, and what antibodies do Innate defenses are fast and generic; acquired defenses are slower to start but specific and remembered. Antibodies are tags and clumpers, not killers — they mark work for phagocytes, complement, and killer cells.

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.

time / exposures → antibody → 1st: slow, small 2nd: fast, big (IgG) Allergy = IgE misfire mast cell coated in IgE allergen histamine → swelling, itch, leaks
Figure 8 · The memory curve, and allergy as friendly fire Left: the second exposure dwarfs the first — that gap is immune memory, and it's why boosters work. Right: in allergy, IgE-primed mast cells dump histamine when the allergen returns.
Key idea

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.

Blood & Immunology — one-glance recap
White cellsNeutrophils (first responders), macrophages (eat + present), eosinophils (parasites), basophils/mast (histamine), lymphocytes (specific + memory). Exit via diapedesis, home in by chemotaxis.
Lymphatic ↔ immuneLymphatics return leaked fluid and filter it through nodes (antigen checkpoints); spleen filters blood; lymphocytes recirculate. Blocked drainage → edema.
Immune functionsInnate: barriers, phagocytes, complement (tag/recruit/lyse). Acquired: antibodies (neutralize, agglutinate, opsonize) and cytotoxic T-cells; memory persists.
Innate vs. acquired + allergyInnate = fast/general; acquired = specific/remembered (2nd response bigger). Allergy = IgE-coated mast cells releasing histamine on re-exposure.
System 03 — GI Physiology

Gastrointestinal Physiology

Motility · secretion & hormones · enzymes · bile · pancreas · liver · absorption · defecation
You'll be able to…
a Describe the physiology of GI motility, gastric secretion, and gastric hormones.
b Describe digestive enzymes of the GI tract.
c Describe the function of the biliary system.
d Describe the exocrine function of the pancreas.
e Describe the functions of the liver.
f Describe protein, carbohydrates, and lipid absorption.
g Explain the process of defecation.

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).

Peristalsis — pushes forward Segmentation — mixes in place GASTRIN from: stomach (G-cells) trigger: protein, stretch does: ↑ acid + ↑ motility SECRETIN from: duodenum trigger: acid in duodenum does: pancreatic bicarb CCK from: duodenum trigger: fat / protein does: gallbladder + enzymes, slows emptying
Figure 9 · Two moves, three messengers Peristalsis is the conveyor belt; segmentation is the mixer. Memorize the three hormones by their trigger: acid in the duodenum calls secretin (bicarbonate to neutralize), fat/protein calls CCK (bile + enzymes), and food in the stomach calls gastrin (acid + motility).

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.

MOUTH STOMACH SMALL INTESTINE Carbs amylase pancreatic amylase → disaccharidases Protein pepsin (acid) proteases → brush-border peptidases Fat bile emulsifies → lipase Enzymes are secreted inactive (zymogens) and activated in the lumen — so the pancreas doesn't digest itself.
Figure 10 · The digestion relay Read left to right: each nutrient is handed from one site to the next. The one rule that ties it together — the powerful proteases are released as inactive zymogens and switched on only after they reach the gut, protecting the pancreas from self-digestion.

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.

livermakes bile gallbladderstores/concentrates pancreasbicarb + enzymes duodenum(mixing bowl) Bile emulsifies fat big fat drop many small drops = more surface for lipase
Figure 11 · Three tributaries into the duodenum Liver, gallbladder, and pancreas all drain into the duodenum. Bile's trick is emulsification — breaking one big fat globule into many small droplets multiplies the surface area lipase can act on.

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).

gut absorbsnutrients portal vein LIVERfirst pass ateverything rest of body glucose buffer detox / urea bile + proteins store Fe/vitamins Kupffer filter
Figure 12 · Everything passes through first The portal vein routes gut blood through the liver before it reaches the body — the anatomical reason the liver is the metabolic gatekeeper, doing first-pass processing of nutrients and toxins alike.

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.

intestinal cell LUMEN (food) glucose,amino acids Na⁺-coupled BLOOD→ liver fats (in bile-salt micelles) → chylomicrons LYMPH→ blood later
Figure 13 · Two exits from the gut cell Water-soluble nutrients (sugars, amino acids) take the blood/portal route straight to the liver. Fat takes the scenic route — repackaged as chylomicrons into lymph first, because the particles are too big for blood capillaries.

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.

Key idea

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.

GI Physiology — one-glance recap
Motility & hormonesEnteric NS + slow waves. Peristalsis pushes, segmentation mixes. Gastrin (acid+motility), secretin (bicarbonate for acid), CCK (bile+enzymes for fat).
EnzymesCarbs: amylase → disaccharidases. Protein: pepsin (acid) → proteases/peptidases. Fat: bile + lipase. Proteases secreted as zymogens.
Bile & pancreasLiver makes bile; gallbladder stores/concentrates; CCK releases it; amphipathic bile salts emulsify fat; recycled in ileum. Pancreas: bicarbonate (secretin) + enzymes (CCK).
LiverFirst-pass via portal vein: glucose buffer, detox, urea, bile, plasma proteins, storage, Kupffer filtering.
AbsorptionVilli/microvilli surface. Sugars & amino acids: Na⁺-coupled → blood → liver. Fat: micelles → chylomicrons → lymph → blood.
DefecationGastrocolic reflex → mass movement. Internal sphincter (involuntary) relaxes; external sphincter (voluntary) allows delay.
System 04 — Chapters 68–71

Metabolism & the Liver

The liver's jobs · making and moving glucose, fat, and protein
You'll be able to…
a Review the functions of the liver.
b Describe the production, transport, and conversion of glucose.
c Describe the production, transport, and conversion of lipids.
d Describe the production, transport, and conversion of protein.

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.

glycolysis · 2 ATP citric acidcycle oxidative phosphorylationmost of the ATP(needs oxygen) no O₂ needed O₂ required · big payoff
Figure 14 · The energy staircase Glycolysis gives a quick, small payout with no oxygen; the citric acid cycle preps the fuel; oxidative phosphorylation, using oxygen, releases the overwhelming majority of the ATP. This is why oxygen matters so much to energy supply.

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).

LIVER+ gut (dietary fat) TISSUESuse / store fat deliver out: chylomicrons, VLDL, LDL HDL returns excess cholesterol back to liver Fasting: livermakes ketones(brain fuel)
Figure 15 · Fat has a delivery fleet Chylomicrons, VLDL, and LDL carry fat and cholesterol outward to tissues; HDL is the return truck bringing excess cholesterol back. Remember direction: LDL = Leaves (to tissues), HDL = Heads home (to liver).

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.

amino acidfrom the pool build protein burn skeletonfor energy remove N first nitrogen → urea (liver)→ kidneys GH builds ·cortisol breaks down
Figure 16 · Build it or burn it — but handle the nitrogen An amino acid is either used to build protein or stripped of its nitrogen so the carbon skeleton can be burned. The stripped-off nitrogen is toxic, so the liver locks it into urea for safe excretion.
Key idea

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.

Metabolism & the Liver — one-glance recap
Liver functionsGlucose buffer, detox + urea, bile, plasma proteins, storage; first-pass via portal vein.
GlucoseGlycolysis (2 ATP, no O₂) → citric acid cycle → oxidative phosphorylation (most ATP, needs O₂). Insulin lowers, glucagon raises; gluconeogenesis feeds the glucose-dependent brain.
LipidsBeta-oxidation → acetyl-CoA; fasting → ketones. Transport: chylomicrons (diet), VLDL (liver out), LDL (to tissues), HDL (back to liver).
ProteinAmino-acid pool; deamination/transamination frees the skeleton; urea cycle disposes nitrogen. Last-resort fuel. GH anabolic, cortisol catabolic.
System 05 — Chapters 72–74

Nutrition, Energetics & Thermoregulation

Energy balance · body temperature control · metabolic rate
You'll be able to…
a Discuss body energy balance.
b Analyze body temperature and how it is controlled.
c Discuss metabolic rate.

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).

energy in energy out surplus → stored as fat Fuel stores, by size Fat — huge (weeks) Glycogen — small (~1 day) Glucose — tiny (minutes) Starvation order: glycogen → fat → (last) protein
Figure 17 · The ledger and the pantry Weight change is just in-minus-out. The pantry is lopsided: fat is the warehouse, glycogen a day's shelf, glucose a snack on the counter — which sets the order the body burns them in when food stops.

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.

hypothalamusset point ≈ 37 °C TOO COLDvasoconstrict,shiver (make heat) TOO HOTvasodilate,sweat (lose heat) Heat leaves by: radiation · conduction · convection · evaporation Fever = set point pushed higher (chills to reach it); "breaks" = set point drops (flush & sweat).
Figure 18 · A thermostat that can be reset Too cold, the hypothalamus makes and keeps heat; too hot, it sheds it. Fever is the same machinery aimed at a higher target — which is why you shiver on the way up and sweat on the way down.

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.

Where a day's energy goes Basal metabolic rate (biggest slice) activity (variable) food Raises rate ↑ thyroid hormone · sympathetic activity · larger body · fever Lowers rate ↓ aging (less muscle) · rest / sleep Fuel readout — respiratory quotient: ~1.0 carbohydrate, ~0.7 fat
Figure 19 · The energy budget Most of your daily calories just keep the resting body alive (BMR); activity is the lever you control; digesting food costs a little extra. Thyroid and sympathetic drive turn the whole thing up.
Key idea

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.

Nutrition, Energetics & Thermoregulation — one-glance recap
Energy balanceIn 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.
TemperatureHypothalamic set point ≈ 37 °C. Cold: vasoconstrict + shiver. Hot: vasodilate + sweat (evaporation cools). Loss: radiation, conduction, convection, evaporation. Fever = raised set point.
Metabolic rateBMR = largest slice (measured rested/fasting). + activity + thermic effect of food. ↑ thyroid, sympathetic, body size; ↓ with age. RQ: 1.0 carb, 0.7 fat.
System 06 — Chapters 38–40

Respiration I — Ventilation & Gas Exchange

Breathing muscles · compliance · lung volumes · surfactant · gas exchange · the membrane
You'll be able to…
a Compare and contrast the functions of the muscles of respiration.
b Explain compliance and elasticity of lung.
c Compare and contrast lung capacities and lung volumes.
d Describe the function of surfactant.
e Explain gas exchange taking place in the lungs.
f Review the respiratory membrane.

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.

Rest diaphragm up Inspiration diaphragm contracts & drops air in Boyle's law volume ↑ pressure ↓ air flows in Negative pleural pressure keeps the lung open.
Figure 20 · Make the box bigger, air rushes in The diaphragm drops, the chest enlarges, pressure falls below the outside air, and air flows in — no pump required, just Boyle's law. The lung stays open the rest of the time because the pleural space is held at a slight vacuum.

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).

← tidal volume (normal breath) IRV tidal ERV residual (can't exhale) vital capacity Total lung capacity = every volume incl. residual · Vital capacity = all you can move (excl. residual)
Figure 21 · One breath, and the reserves around it A normal breath (tidal) sits in the middle; you can inhale more (IRV) or exhale more (ERV) on demand. What's left after a full exhale — residual volume — never leaves, so a spirometer can't measure it.

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.

Without surfactant small — high tension empties into big With surfactant both stable & open · easy to inflate
Figure 22 · Why small sacs need help Surface tension hits small alveoli hardest, so without surfactant they'd deflate into larger ones. Surfactant lowers tension most where it's needed, stabilizing the small sacs and making the whole lung easier to expand.

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.

ALVEOLUS (air)O₂ high · CO₂ low CAPILLARY (blood)O₂ low · CO₂ high thin membrane O₂ → ← CO₂
Figure 23 · Downhill both ways Each gas simply rolls down its own pressure gradient — O₂ into blood, CO₂ out — across a membrane so thin and so vast that exchange finishes with room to spare. Add fluid (thicker barrier) and the whole thing slows.
Key idea

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.

Respiration I — one-glance recap
MusclesDiaphragm (phrenic nerve) for quiet breathing; accessory muscles for forced. Contract → volume ↑ → pressure ↓ → air in (Boyle's law).
Compliance/elasticityCompliance = ease of inflation; elastic recoil pulls inward; negative intrapleural pressure holds lungs open; pneumothorax → collapse.
Volumes/capacitiesTidal + IRV + ERV + residual. Residual can't be exhaled (spirometry misses it). VC = movable air; TLC = everything.
SurfactantLowers surface tension (most in small alveoli) → raises compliance, prevents collapse (Laplace).
Gas exchange / membraneDiffusion down partial-pressure gradients; O₂ in, CO₂ out; complete with safety margin. Fast because area is huge and membrane thin; CO₂ crosses easily (soluble).
System 07 — Chapters 41–42

Respiration II — Gas Transport & Control

Respiratory centers · O₂ transport · CO₂ transport · breathing & pH · tissue exchange
You'll be able to…
a Compare and contrast the respiratory centers of the brain.
b Describe oxygen transport within the cardiopulmonary circulation.
c Describe carbon dioxide transport within the cardiopulmonary circulation.
d Describe respiratory influence on pH.
e Describe gas exchange at the tissue level.

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.

medullamakes the rhythm pons — smooths it central chemoreceptorssense CO₂ → H⁺ (main driver) peripheral chemoreceptorssense low O₂ (backup) CO₂ is thestrongesteveryday signal
Figure 24 · The breathing control room The medulla sets the beat, the pons refines it, and chemoreceptors adjust it. Counter-intuitively, rising CO₂ (sensed as acid) drives breathing far more than falling oxygen, which is the emergency backup.

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.

tissue oxygen (PO₂) → % O₂ on hemoglobin → → right shift (exercise: CO₂, acid, heat) — unloads more O₂ ← left shift (cold, CO, fetal Hb) — holds O₂
Figure 25 · The curve that delivers oxygen on demand At the tissues, the exact conditions of hard work — heat, acid, CO₂ — slide the curve right and loosen hemoglobin's grip, so busy muscle automatically gets more oxygen. This tissue-level unloading is objective (e) in action.

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.

~70% bicarbonate(via carbonic anhydrase) ~23% on hemoglobin(carbamino — on globin) ~7% dissolved(free in plasma) bicarbonate out → chloride in (chloride shift)
Figure 26 · CO₂'s three rides Most CO₂ is quietly carried as bicarbonate — the same chemistry that links breathing to acid-base balance. Only a fifth rides on hemoglobin, and just a sliver is dissolved.

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 + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻ hyperventilateblow off CO₂ → alkalosis hypoventilateretain CO₂ → acidosis
Figure 27 · Breathing as a pH lever CO₂ is an acid in disguise. Breathe it off and blood turns alkaline; hold it in and blood turns acidic. The lungs are the fast lever on pH; the kidneys are the slow, thorough one.
Key idea

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.

Respiration II — one-glance recap
Control centersMedulla 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 & pHCO₂ + H₂O ⇌ H⁺ + HCO₃⁻. Hyperventilation → alkalosis; hypoventilation → acidosis. Lungs fast, kidneys slow/thorough.
Tissue exchangeLow tissue PO₂ → O₂ diffuses out; high tissue PCO₂ → CO₂ diffuses in; right-shifted curve boosts unloading in active tissue.