CHAPTER 12
DISCUSSION OF CASE STUDY 12.1
Helen has taken an overdose of aspirin. She has a metabolic acidosis being
compensated by the hyperventilation. Initially, such patients present with
a respiratory alkalosis and this is followed by a metabolic acidosis. The
prothrombin time (Chapter 13) is prolonged due to decreased hepatic
activation of clotting factors. Helen’s treatment will be supportive and may
include gastric lavage for up to 24 h after ingestion, possibly oral activated
charcoal and infusions of sodium hydrogen carbonate to promote excretion
of salicylate. Hemodialysis is not required, given the concentration of
salicylate in Helen’s plasma.
DISCUSSION OF CASE STUDY 12.2
Olga had taken a paracetamol overdose with vodka. Liver function tests were
not abnormal on admission. The transient elevation of the plasma alanine
aminotransferase suggests that some mild degree of liver damage had taken
place. The time of the paracetamol overdose was not known accurately.
Olga was treated with intravenous N-acetylcysteine. She should also receive
counseling regarding the problems that led to the attempted suicide.
DISCUSSION OF CASE STUDY 12.3
Edward’s abnormal clotting time and high bilirubin and alkaline phosphatase
levels indicate a serious derangement of liver function. He probably has
advanced cirrhosis of the liver. Extensive fibrosis of the liver has distorted
the intraheptic bilary tree increasing the bilirubin and alkaline phosphatase
levels (whose synthesis is induced by alcohol). F-glutamyltransferase activity
is frequently used as a marker for excessive alcohol consumption since its
synthesis is also induced by alcohol. However, the test is not specific since
F-glutamyltransferase can also be induced by a number of drugs including
some antiepileptics and oral contraceptives. Hyperbilirubinemia is not always
a feature of chronic liver disease and can occur in other disease states.
Maureen would seem to have moderate alcoholic liver disease but she
shows a somewhat different pattern in the liver function tests. Her GGT
level is clearly increased and the transaminases are also abnormal but her
bilirubin and alkaline phosphatase levels are only slightly above normal.
Even relatively moderate levels of alcohol can produce structural changes in
the liver cells including accumulation of fatty droplets, proliferation of the
endoplasmic reticulum and enlargement of the mitochondria.
DISCUSSION OF CASE STUDY 12.4
The high [H+] and low HCO 3 – indicate a metabolic acidosis (Chapter 9) due
to increased production of lactate from poisoning with carbon monoxide.
Carbon monoxide binds more avidly to hemoglobin than oxygen and
decreases the ability of hemoglobin to transport oxygen. John was
unconscious because of reduced delivery of oxygen to his brain. John can be
treated with hyperbaric oxygen. The high PO 2 causes displacement of carbon
monoxide from hemoglobin.
CHAPTER 13
DISCUSSION OF CASE STUDY 13.1
Daniel clearly has sickle cell anemia and is homozygous for the condition.
Both parents are heterozygotes and carry the sickle cell trait. Sickle cell
individuals experience severe pain and need to be given strong painkillers.
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