Unit 06 · Digestive & Urinary Systems

Food passes mouth → pharynx → esophagus → stomach → small intestine → large intestine → rectum → anus. Mechanical breakdown and mixing increase access; chemical digestion hydrolyzes molecules. The liver makes bile, the gallbladder stores/concentrates it, and the exocrine pancreas supplies enzymes and bicarbonate. Bile helps emulsify fats but is not an enzyme. Pancreatic endocrine hormones enter blood, not the food tube.

Villi and enterocyte microvilli expand exchange area. Most carbohydrate digestion products and amino acids enter villus capillaries and portal blood; most absorbed long-chain lipids are packaged into chylomicrons and enter lacteals before returning to blood. The small intestine absorbs most nutrients and most water; the colon reclaims much of the remaining water. Luminal water includes secretions as well as intake, so a GI-flow ledger is not a drinking-water prescription.

In a kidney, cortex surrounds medulla, which contains pyramids draining toward the renal pelvis. Corpuscles are in cortex; loops extend to varying depths toward the medulla. Blood passes renal arterial branches → afferent arteriole → glomerular capillaries → efferent arteriole → peritubular capillaries or vasa recta. Filtrate instead enters Bowman’s space → proximal tubule → nephron loop → distal tubule → connecting segment/collecting duct → papillary outflow → calyces/pelvis → ureter → bladder → urethra. The collecting duct receives fluid from several nephrons; blood does not flow down the tubular lumen.

Filtration moves water and small solutes from glomerular blood into Bowman’s space, driven by net filtration pressure across a selective barrier; cells and most large proteins remain in blood. GFR is filtrate volume per time, not urine output and not the fraction of whole blood that disappears. Hydrostatic and oncotic pressures and the filtration coefficient matter. Autoregulation buffers changes only over a limited range; doubling systemic pressure does not imply doubling GFR.

Reabsorption moves material from tubule toward interstitium and blood; secretion moves material from blood/interstitium into the tubular fluid. Excretion is what leaves in urine. For a freely filtered solute at steady state: excreted amount/time = GFR × plasma concentration − reabsorbed amount/time + secreted amount/time. Distinguish this from concentration: a dilute urine can still contain a substantial daily amount if urine flow is high.

The proximal tubule reclaims much filtered sodium, water, glucose, amino acids, and bicarbonate; apical cotransport uses gradients maintained in part by basolateral sodium-potassium ATPase. Transport capacity is finite. The descending limb is relatively water-permeable; the thick ascending limb reabsorbs salt but is poorly permeable to water. Repeated countercurrent flow and salt transport help build the medullary gradient, while vasa recta countercurrent exchange helps preserve it and urea recycling contributes. A colored model cannot show these transport rates directly.

Later nephron segments fine-tune excretion. ADH is synthesized in the hypothalamus and released from the posterior pituitary; it increases collecting-duct water permeability through aquaporin insertion when the gradient permits water recovery. Aldosterone promotes distal sodium reabsorption and potassium secretion; water retention also depends on water availability, permeability, and other controls. Reduced effective perfusion can stimulate renin, leading through angiotensin to vascular and hormonal effects. Atrial natriuretic peptide favors sodium excretion in an appropriate volume context. These loops are not interchangeable: concentration and circulating volume are different controlled variables.

Sodium salts dominate extracellular osmotic balance, whereas potassium is chiefly intracellular. Changing potassium gradients can change muscle and neuronal electrical behavior (Units 02 and 05), but a single number cannot identify its cause. Kidneys also contribute erythropoietin for red-cell production and activate vitamin D, linking renal function to oxygen carriage and calcium/bone physiology. These are explanatory connections, not diagnoses.

Clearance C = urine concentration × urine flow/plasma concentration is a virtual volume of plasma cleared of a marker per time, not a parcel of plasma physically removed. Clearance equals GFR only for a freely filtered marker that is neither reabsorbed nor secreted or otherwise produced/lost by the kidney, with appropriate steady state and complete timed collection assumed. Secretion raises a marker’s clearance above GFR; reabsorption lowers it. The second record explicitly violates the ideal-marker assumption.

In the two-compartment model, water equilibrates across cell membranes, intracellular solute stays intracellular, and the stipulated extracellular solute stays extracellular. Losing pure water concentrates both compartments and shifts water out of cells. Losing an isosmotic extracellular solution removes water and solute together and chiefly contracts extracellular volume without that osmotic shift. The values below omit ongoing intake/output, osmotically inactive stores, active regulation, and nonideal solution effects; they are not a fluid prescription or rehydration plan.

Renal acid-base regulation includes reclaiming filtered bicarbonate and excreting acid with buffers such as phosphate and ammonium. Reclaiming previously filtered bicarbonate prevents its loss; net acid excretion can be associated with adding new bicarbonate to blood. In the supplied balance, net acid excretion = ammonium + titratable acid − bicarbonate excretion, with all terms expressed as H+ equivalents. Urine pH alone cannot reveal this total because it does not count buffered acid or urine volume. Respiratory compensation has its own limits and time scale, as Unit 04 showed.

SGLT1 and SGLT2 are sodium-glucose cotransporters, not ATP-hydrolyzing pumps. Apical SGLT2 supports bulk glucose recovery in the early proximal tubule; SGLT1 supports recovery later in the proximal tubule and also absorbs glucose and galactose in the intestinal brush border. SGLT1 is commonly described as higher-affinity/lower-capacity and SGLT2 as lower-affinity/higher-capacity in this comparison, but measured values depend on conditions and expression. They are not interchangeable with GLUT5, which facilitates intestinal fructose entry, or GLUT2, which supports basolateral glucose exit in enterocytes and early proximal cells.

This is secondary active transport: downhill sodium movement can drive uphill glucose entry. The basolateral sodium-potassium ATPase spends ATP to maintain the sodium gradient; SGLT does not directly split ATP on each glucose-transfer step. If that electrochemical driving force changes, a formula that assumed it fixed no longer predicts the flux. A kidney micrograph cannot reveal either transporter identity or its current activity.

For each isolated ideal membrane patch use J = Jmax × C/(Khalf + C), where C is luminal glucose in mmol/L and J is glucose flux in nmol per square centimetre per minute. The invented constants describe separate SGLT1-only and SGLT2-only patches with fixed transporter abundance, sodium gradient, voltage, temperature, and rapid steady state. They are not measured human kinetic constants. Khalf is the C giving half that patch’s limiting flux; a smaller value does not by itself guarantee greater flux at every concentration. The limit Jmax is approached, not exactly attained at finite C in this equation.

The separate aggregate kidney model uses plasma concentration P in mg/mL, GFR in mL/min, and an ideal total glucose-reabsorption capacity Tm in mg/min. Filtered F = P × GFR; reabsorbed R = min(F, Tm); excreted E = F − R. Assume freely filtered glucose, no secretion, no synthesis or metabolism within the modeled accounting boundary, and steady state. Plasma P is not the luminal C in the isolated-patch experiment. Tm is not Khalf, and adding patch Jmax values without membrane areas or segment delivery would be dimensionally wrong.

The sharp corner at P = Tm/GFR assumes identical nephrons and complete recovery below capacity. Real excretion can begin gradually before a whole-kidney plateau: this rounded transition is called splay and reflects heterogeneous delivery/capacity and non-instantaneous saturation. The two-group toy model demonstrates heterogeneity only, not the complete renal curve. These are educational ledgers, not real tests, diagnostic thresholds, clinical dosing, or treatment advice.