CASE 1

A 48-year-old male presents to the clinic because of concerns about heart disease. He reports
that his father died from a heart attack at age 46, and his older brother has also had a heart
attack at age 46 but survived and is on medications for elevated cholesterol. The patient
reports chest pain occasionally ith ambulation around his house and is not able to climb
stairs ithout significant chest pain and shortness of breath. The physical e!am is normal,
and the physician orders an electrocardiogram "#$%&, e!ercise stress test, and blood ork.
The patient's cholesterol result comes back as ()* mg+d, "normal -**&. The physician
prescribes medication, hich he states is directed at the ratelimiting step of cholesterol
biosynthesis.
What is the rate-limiting step of cholesterol metabolism?
What is the class of medication prescribed?
CASE 2 ()
Lofata Brne is a .6-year-old girl. /ince age .4 months she has e!perienced recurrent
episodes of profound fatigue associated ith vomiting and increased perspiration, hich
re0uired hospitali1ation. These episodes occurred only if she fasted for more than 8 hours.
2ecause her mother gave her food late at night and oke her early in the morning for
breakfast, ,ofata's physical and mental development had progressed normally.3n the day of
admission for this episode, ,ofata had missed breakfast, and by noon she as e!tremely
fatigued, nauseated, seaty, and limp. /he as unable to hold any food in her stomach and
as rushed to the hospital, here an infusion of glucose as started intravenously. Her
symptoms responded dramatically to this therapy.
Her initial serum glucose level as lo at (8 mg+d, "reference range for fasting serum
glucose levels 4 5*6.**&. Her blood urea nitrogen "278& level as slightly elevated at -6
mg+d, "reference range 4 86-)& as a result of vomiting, hich led to a degree of dehydration.
Her blood levels of liver transaminases ere slightly elevated, although her liver as not
palpably enlarged. 9espite elevated levels of free fatty acids "4.( m:& in the blood, blood
ketone bodies ere belo normal. What happened !ith Lofata Brne?
CASE "
A 6(-year-old female presents to the clinic ith recurrent midepigastric pain over the last (
months. /he reports some relief shortly after eating, but then the discomfort returns. /he has
tried various over-the-counter medications ithout relief. /he also reports feeling tired and
has had to increase the amount of ibuprofen needed for relief of her arthritis. /he denies
nausea, vomiting, and diarrhea. 3n e!am she is found to have mild midepigastric tenderness
and guaiac positive stool. A $2$ revealed a microcytic anemia and normal hite blood cell
count, consistent ith iron deficiency. The patient as referred to a gastroenterologist ho
performed an upper %; endoscopy that identified gastric ulcers. He stated that he suspected
that the ibuprofen, a nonsteroidal antiinflammatory drug "8/A;9& as the causative agent
and suggested sitching from ibuprofen to a co!ib, such as celeco!ib.
What is the li#el$ biochemical etiolog$ of the disorder?
Wh$ do co%ibs generall$ ha&e a lo!er incidence of pper '( problems than other
)SA(*s?
What is the ma+or difference bet!een aspirin and other )SA(*s !ith regard to
platelet fnction?
CASE , ()
*iana, a -5-year-old oman ith type . diabetes mellitus, had been admitted to the hospital
in a ketoacidotic coma a year ago. /he had been feeling drosy and had been vomiting for -4
hours before that admission. At the time of admission, she as clinically dehydrated, her
blood pressure as lo, and her breathing as deep and rapid "<ussmaul breathing&. Her
pulse as rapid, and her breath had the odor of acetone. Her arterial blood pH as 5.*8
"reference range, 5.(65.44&, and her blood ketone body levels ere .) m: "normal is
appro!imately *.- m: for a person on a normal diet&. What happened !ith *iana?
CASE - ()
/ince her admission to the hospital for an acute myocardial infarction, Ann .eina has been
taking the bile salt se0uestrant cholestyramine and the H:%-$oA reductase inhibitor
pravastatin to loer her blood cholesterol levels. /he also takes .6* mg acetylsalicylic acid
"A/A= aspirin& each day. At her most recent visit to her cardiologist, she asked hether she
should continue to take aspirin because she no longer has any chest pain. /he as told that
the use of aspirin in her case as not to alleviate pain but to reduce the risk of a second heart
attack and that she should continue to take this drug for the remainder of her life unless a
complication, such as gastrointestinal bleeding, occurred as a result of its use. What
happened !ith Ann .eina?
CASE / ()
Emma Whee0er has done ell ith regard to her respiratory function since her earlier
hospitali1ation for an acute asthmatic attack. /he has been maintained on to puffs of
triamcinolone acetonide, a potent inhaled corticosteroid, three times per day, and has not
re0uired systemic steroids for months. The glucose intolerance precipitated by high
intravenous and oral doses of the synthetic glucocorticoid de!amethasone during her earlier
hospitali1ation resolved after this drug as discontinued. /he has come to her doctor no
because she is concerned that the lo-grade fever and cough she has developed over the last
(6 hours may trigger another acute asthma attack. What happened !ith Emma Whee0er?