Enzymes

Why this matters

Caries is an enzyme problem: without glucosyltransferase, sucrose would not build plaque. Half the prescriptions you write are enzyme inhibitors, and the ones that hurt patients do so by colliding with a drug-metabolising enzyme. A child who loses primary teeth with the roots still on them has an enzyme deficiency. You will read an alkaline phosphatase result and be expected to know what it means.

The big picture

An enzyme is a protein that holds a reaction's transition state more tightly than it holds the substrate. That one idea explains everything else: why active sites are shaped the way they are, why inhibitors that mimic the transition state are so potent, and why an enzyme can make a reaction a hundred thousand billion times faster without shifting its equilibrium a single step.

The 14 cards in this lesson

1. 01What an enzyme changes, and what it cannot
2. 02The active site is small, and it moves
3. 03How a protease actually cuts
4. 04Seven classes, and where you meet them
5. 05Michaelis-Menten: the saturation curve
6. 06Km is not simply affinity
7. 07Four kinds of inhibition, and how to tell them apart
8. 08Clinical alert — in the lesson
9. 09Cofactors, and the mouth signs when they run out
10. 10Made inactive on purpose: zymogens
11. 11The other four ways to control an enzyme
12. 12The enzymes that cause caries
13. 13Clinical alert — in the lesson
14. 14Clinical alert — in the lesson

You have got it when

You are ready to continue when you can say exactly what an enzyme does and does not change, read a Lineweaver-Burk plot and name the type of inhibition, and explain why miconazole gel is dangerous in a patient on warfarin.