Biochemistry — Energy, Nitrogen and Lipids, NMC MBBS licence examination syllabus (Nepal Medical Council).
Energy, Nitrogen and Lipids
A rising lactate is a biochemistry result that tells you the patient's tissues are not getting enough blood. Almost nothing else on the sheet says that so directly.
The first biochemistry chapter covered the fed–fasting switch and what happens when a metabolic step is blocked. This one covers three processes whose failure you will see on a results sheet several times a week: energy production, nitrogen disposal, and lipid transport.
Pathways are described here by what they achieve and what their failure looks like, not as diagrams to reproduce. Nothing in a licensing examination depends on naming an intermediate.
Energy with and without oxygen
Glucose breakdown happens in two stages, and the split between them is the clinically useful part.
The first stage needs no oxygen. Glucose is split, and a small amount of energy is released. This runs in every cell, all the time, whatever the oxygen supply.
What happens next depends on oxygen. With oxygen available, the products enter the mitochondria and are broken down completely, releasing far more energy and producing carbon dioxide and water. Without oxygen, the sequence stops early and the leftover product is converted to lactate.
That is why lactate is a perfusion marker. A rising lactate means tissue somewhere is producing energy without enough oxygen — which in a sick patient usually means it is not receiving enough blood. This is the reason lactate is measured and followed in sepsis and shock, and why a falling lactate is taken as evidence that resuscitation is working. It is biochemistry doing bedside work.
Two qualifications worth knowing. Lactate also rises from vigorous muscular activity, including a prolonged seizure, without any circulatory failure. And a failing liver clears lactate poorly, so liver disease raises it for a different reason. As always, the number is interpreted alongside the patient.
Nitrogen: why liver failure affects the brain
Carbohydrate and fat contain carbon, hydrogen and oxygen, and burning them produces carbon dioxide and water — both easily disposed of. Protein additionally contains nitrogen, and that creates a problem.
Breaking down amino acids releases ammonia, which is toxic, particularly to the brain. The liver converts ammonia into urea, which is harmless and water-soluble, and the kidney excretes it.
So a failing liver cannot dispose of nitrogen, ammonia accumulates, and the brain is affected. That is a substantial part of hepatic encephalopathy — the confusion, drowsiness and eventual coma of advanced liver disease.
💡 This explains a clinical association that otherwise looks arbitrary: a gastrointestinal bleed precipitates encephalopathy in a patient with cirrhosis. Blood in the gut is a large protein meal. Digesting it delivers a heavy nitrogen load to a liver that was only just coping — so a patient who was stable becomes confused. Knowing the mechanism means you anticipate it rather than being surprised by it.
The same pathway explains the inherited disorders introduced in the first chapter: a defect in the urea cycle leaves a newborn unable to clear the nitrogen from their first feeds, which is why they are well at birth and deteriorate once feeding starts.
Bilirubin: where did the process break?
Bilirubin comes from the breakdown of haemoglobin. It arrives at the liver unconjugated — fat-soluble and not excretable — and the liver conjugates it, making it water-soluble so it can be passed into bile and out through the gut.
Jaundice means that process has broken, and where it broke produces three recognisable patterns:
Too much arriving — haemolysis. The liver is normal but overwhelmed, so unconjugated bilirubin rises. Since unconjugated bilirubin cannot enter urine, the urine stays normal, and bile still reaches the gut so stools stay normal.
The liver cannot process it — hepatocellular disease. A mixed picture, with transaminases raised because hepatocytes are damaged and leaking.
It cannot get out — obstruction. Conjugated bilirubin rises. Because it is water-soluble it spills into urine, making it dark; because bile cannot reach the gut, stools become pale. Itching is common.
The dark urine and pale stools of obstruction are not an arbitrary pairing to memorise — they are two consequences of the same fact. Conjugation makes bilirubin water-soluble, so only the conjugated form can appear in urine, and only bile reaching the gut can colour the stool. One piece of chemistry, two clinical signs.
Why the form matters in a newborn
The distinction between conjugated and unconjugated is not merely a laboratory classification. In a newborn it determines the danger.
Unconjugated bilirubin is fat-soluble, so it can cross into the brain. Conjugated bilirubin is water-soluble and cannot. High levels of unconjugated bilirubin in a newborn can therefore cause permanent brain injury.
Two facts make newborns vulnerable: the immature liver conjugates slowly, which is why physiological jaundice exists at all, and prematurity makes it slower still.
Phototherapy works by converting bilirubin in the skin into forms that can be excreted without being conjugated — bypassing the immature liver entirely. That is why light treats a chemical problem, which otherwise seems an odd pairing. The clinical thresholds and management are covered in the neonatology chapter and are chart-based, varying with gestation and postnatal age, so no values appear here.
Lipids: the direction of travel
Fat does not dissolve in blood. So it is carried in lipoproteins — particles with a fatty core wrapped in a water-compatible shell — and the shell determines where the particle goes and what it does.
LDL carries cholesterol outward, from the liver to the tissues, including the walls of arteries. Higher LDL means more cholesterol delivered where atheroma forms, so higher cardiovascular risk.
HDL carries cholesterol back, from the tissues to the liver for disposal. Higher HDL is associated with lower risk.
The popular labels "good" and "bad" cholesterol are misleading in a way worth correcting: it is the same cholesterol molecule in both. What differs is the direction it is being carried. Understanding it that way makes the risk relationship obvious rather than arbitrary — and connects directly to the pathology chapter, where cholesterol delivered into an arterial wall becomes the lipid core of a plaque.
Cholesterol is not a poison. It is a required component of every cell membrane and the starting material for steroid hormones, vitamin D and bile acids — which is why the body makes its own rather than relying on diet, and why dietary change alone shifts blood levels less than patients expect.
No target values appear in this chapter: they differ between guidelines, are revised, and depend on the patient's overall cardiovascular risk rather than on a single threshold.
Putting it together
Energy production without oxygen produces lactate, so a rising lactate means tissue is under-perfused — with liver failure and seizure as the two qualifications.
Protein leaves nitrogen behind, the liver converts ammonia to urea, and failure of that causes encephalopathy.
A GI bleed is a protein meal, which is why it precipitates encephalopathy in cirrhosis.
Conjugation makes bilirubin water-soluble — which is why obstruction gives dark urine and pale stools.
Unconjugated bilirubin crosses into the brain, and phototherapy bypasses the immature liver.
LDL carries cholesterol out, HDL brings it back. The same molecule, opposite directions.
No ATP yields, pathway intermediates, lipid targets or bilirubin thresholds appear here: yields are contested between textbooks, targets differ between guidelines, and neonatal thresholds are chart-based and vary with gestation. Use your current guideline.
Syllabus points
Energy with and without oxygen; lactate
Lactate as a perfusion marker, and its two qualifications
Ammonia, urea and hepatic encephalopathy
Why a GI bleed precipitates encephalopathy
Three patterns of jaundice
Conjugation explains dark urine and pale stools
Unconjugated bilirubin and the newborn brain
LDL out, HDL back — the same molecule
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