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The liver has a substantial normal range of size, determined by age, body dimensions, nutritional state and its variable contents; there is no universal absolute minimum and maximum valid for every healthy person. One must also distinguish true organ volume from the position of its lower border, which moves with the respiratory diaphragm during breathing.

An ordinary adult liver is on the order of 1.5 kg and roughly a few percent of body mass, but neither figure is a diagnostic boundary. As an explicitly modern example, an autopsy study of adult men reported a mean hepatic mass of 1561 g and observed values from 838 to 2584 g in its selected population. Those are sample observations, not a declaration that every liver inside those limits is healthy or that every one outside is diseased. A newer large-sample study similarly found an association of liver mass with body mass; much of an apparent sex difference disappears when body size is taken into account.^[ref][ref]

Age changes the proportion as well as the absolute size. The fetal and infant liver is relatively large; the adult organ is smaller in proportion to the whole body. Its fetal role in haematopoiesis and subsequent changes of growth and function make an adult mass standard inappropriate for an infant. Constitutional body size and normal anatomical shape also vary: a long lower projection is not necessarily the same thing as an enlarged total organ.

Reversible differences within one person arise because the liver is a store and a vascular organ:

A meal therefore changes hepatic activity and splanchnic blood flow without requiring a large immediate increase in total liver volume. In a modern paired study of 20 healthy volunteers, single-photon emission computed tomography before and after a standardized meal showed a nonsignificant 1.5% decrease in estimated liver volume. The authors judged the change to be within methodological error. This is a useful check against assuming that greater digestive activity proves gross swelling.^[ref]

The experimental approach is to compare like with like: specify age and body mass, use a fixed interval after food, standardize hydration, posture and respiratory phase, and distinguish a volume measurement from a palpable edge or a single linear dimension. Magnetic resonance imaging can measure volume while magnetic resonance spectroscopy measures glycogen or lipid signals; the two observations answer different questions. The size of an excised organ additionally depends on how much blood remains in it. The physiological point appropriate to the 1866 question is reversible variation with growth, alimentation and vascular filling. Modern imaging results refine that point; they are not numerical standards that the historical exam could have expected.

The liver is both a metabolic processing organ and the producer of bile. These functions must be distinguished: much of what the liver contributes to the body enters the blood, whereas bile is its secretion into the digestive system.

Portal venous blood brings absorbed materials from the alimentary organs to the liver, while the hepatic artery supplies oxygenated blood. Within the hepatic sinusoids, the incoming blood encounters hepatocytes and scavenging Kupffer cells. Hepatocytes take up, transform, store and release substances; their bile canaliculi conduct bile towards the bile ducts. The organ's position therefore makes it a useful regulator between absorption from a meal and supply to the rest of the body.

Its main non-biliary functions include the following:

This modern list extends beyond the knowledge and biochemical vocabulary of 1867. It is consistent with the organ's combined metabolic, storage and clearance roles, rather than treating bile production as the whole explanation.^[ref]

Bile contains water, electrolytes, bile salts, phospholipids, cholesterol and bilirubin conjugates. Hepatocytes form the primary secretion; ductal epithelium modifies it. The gallbladder stores and concentrates bile between meals and releases it into the duodenum. Production of bile must therefore be distinguished from its intermittent delivery to a meal.

Its two central functions are assistance with lipid digestion and nutrient absorption, and excretion of selected waste substances. Amphipathic bile salts help disperse dietary fat and form mixed micelles carrying products of lipid digestion to the absorptive surface of the small intestine. They thereby promote uptake of fatty acids, monoglycerides, cholesterol and fat-soluble vitamins. Bile is not itself a source of pancreatic lipase, nor does emulsification chemically hydrolyse triglycerides. Biliary bilirubin, produced through haem breakdown, provides an excretory route; cholesterol and selected other substances also leave in bile. Most secreted bile salts are recovered, especially in the terminal ileum, and return through the portal vein: the enterohepatic circulation conserves the useful detergent.^[ref]

Two comparisons reveal why both sorts of function matter. First, compare a fresh liver extract with an extract prepared after an appropriate controlled interval: testing for reducing sugar and isolating glycogen distinguishes a stored precursor from newly liberated glucose. A reliable interpretation needs prompt sampling and controls because post-mortem glycogenolysis can change the result after the animal has died; detecting sugar in an organ alone does not prove where all of it was made. Secondly, in classical biliary fistula observations, diverting bile away from the intestine while collecting it separately allowed its output to be measured and the loss of normal fat assimilation to be examined. Comparing faecal fat with and without delivery of bile distinguishes a digestive contribution from a merely excretory one. The modern explanation is that loss of intestinal bile salts impairs mixed micelle formation, while jaundice from retained biliary pigment is a separate consequence of failed pigment elimination.

Historical “amyloid disease” denotes the waxy or lardaceous visceral change, especially in the spleen, liver and kidneys; modern amyloidosis denotes deposition of misfolded protein fibrils. The old descriptive appearance and the modern chemical explanation must be kept distinct.

In nineteenth-century usage the affected organs could be enlarged, firm and unusually translucent or wax-like on section. The name amyloid means starch-like. The historical chemical argument relied on colour reactions with iodine and sulfuric acid, suggesting affinity with starch or cellulose. Such a reaction was a clue to recognition, not a modern identification of the deposited substance. Rudolf Virchow's 1856 account explicitly discusses the waxy change of the spleen, liver and kidneys, and its occurrence with longstanding destructive disease.^[ref]

The three principal visceral examples can be described more precisely:

The distribution is not confined to those three organs. Amyloidosis can also affect the gastrointestinal tract, heart, blood vessels and other sites; the pattern depends on the precursor protein. Modern examples include AA amyloidosis associated with sustained inflammation, AL amyloidosis involving immunoglobulin light chains, and transthyretin amyloidosis. This classification is a present-day explanation, not a list of molecular diagnoses asserted for unnamed 1867 patients.^[ref]

Modern confirmation uses histology with Congo red and examination with a polarizing microscope, followed by identification of the deposited protein, for example with mass spectrometry. The characteristic birefringence supports identification of amyloid; typing distinguishes biologically different diseases. These are later laboratory methods, not apparatus available to the candidate in 1867.^[ref]

Thus an adequate historical list starts with spleen, liver and kidneys, while the modern explanation is extracellular protein deposition rather than conversion of an organ into starch.