The toxic reaction is a delayed one, so the dose must be compared with time since ingestion and apparent symptoms. A patient may be smiling three hours after the dose, but 24 hours later may have lost their liver. Heterozygotes with different mutations on each allele are the most common presenters of this disease. Without functioning copper transporters, ceruloplasm accumulates in the liver where it exerts its toxic effects. Excess copper eventually spills out to brain, cornea, kidney, bones, joints and parathyroid glands.
Patients can initially present with acute fulminant hepatitis, chronic hepatitis, or cirrhosis.
The deficiency leads to pulmonary emphysema, since the lungs have no other defense against tissue-destructive enzymes. Often seen in young, middle aged women. Both homozygotes and heterozygotes may develop cirrhosis and require transplantation. Here s a picture to break things up. You can see it in color in Robbins, pg 870.