Internal-Medicine

Answers: 1–18 113
and bleeding time are usually normal. (Lichtman,
pp. 1870–1871)
8. (E) Hypernephroma, cerebellar hemangiomas,
hepatoma, and giant uterine myomas are the
tumors associated with secondary polycythemia.
Endocrine disorders, hypoxia, and high-affinity
hemoglobins can also cause secondary polycythemia.
(Lichtman, pp. 781–786)
9. (C) Heterophil antibodies react against sheep
red cells and are not absorbed out by the guinea
pig kidney. They are positive in patients with
infectious mononucleosis. In 90% of cases, liver
enzymes are elevated. Examination of the
blood film reveals a lymphocytosis with atypical
lymphocytes. (Lichtman, p. 1137)
10. (A, D, I) Hemoglobin C is abnormal hemoglobin
where lysine has been substituted for glutamic
acid at the sixth position of the
beta-chain. Homozygous C red cells are often
target-shaped with “extra” membrane to make
them less osmotically fragile. However, cells
containing principally HbC are more rigid than
normal and their fragmentation in the circulation
may result in microspherocytes. Intracellular
crystals and oxygenated HbC can be seen. The
spleen is invariably enlarged. Women can
become pregnant and tolerate the pregnancy
well. (Lichtman, p. 684)
11. (B, F, J) Bone lesions in myeloma are destructive,
but the alkaline phosphatase is usually
normal, indicating little blastic activity.
Osteolysis, when combined with immobilization,
can lead to hypercalcemia. It is usually
mediated by an osteoclast-activating factor
from neoplastic myeloma cells in the adjacent
marrow. Bone pain can be severe. Bence Jones
proteinuria and myeloma cells in the marrow
are typical. If cryoglobulinemia occurs, it is
type I. (Lichtman, pp. 1505–1506)
12. (A, D, L) Hemolytic anemias are not associated
with erythroid hypoplasia of the marrow.
Erythroid hyperplasia is present except during
infections or insults that lead to regenerative
crises. As a result, there is usually an increased
number of reticulocytes and elevated fecal and
urinary urobilinogen. Decreased RBC survival is
a hallmark of the disease. (Lichtman, pp. 405–408)
13. (B, H, K) Microcytic hypochromic anemias are
caused by disorders of iron, globin, heme, or
porphyrin metabolism and are not seen in thiamine
deficiency. (Lichtman, pp. 526–527)
14. (D, F, K) Postsplenectomy thrombocytosis usually
resolves within 2 months. Both acute blood
loss and chronic iron deficiency can increase
platelets. Hemolytic anemia is associated with
both increased reticulocytes and thrombocytosis.
Thromboembolic or hemorrhagic phenomena
are more common in essential thrombocytosis
rather than secondary causes. (Lichtman, p. 1785)
15. (C) Iron chelation with desferrioxamine will
reduce the toxicity from iron overload if given
regularly in high doses. The most lethal toxicity
of iron load is iron infiltration of the
myocardium, with resultant dysfunction and
death. (Lichtman, p. 657)
16. (C) Bone marrow examination is most likely to
show increased erythroid-to-myeloid ratio.
Erythroid hyperplasia is common to all hemolytic
anemias, and megaloblastic features may develop
unless folate is supplied. (Lichtman, p. 737)
17. (C) The present treatment of choice for thalassemia
minor is purely supportive. Care is
taken to watch for anemia during intercurrent
illness, due to a regenerative crisis. (Lichtman,
pp. 657–658)
18. (E) Reactive thrombocytosis is usually transitory,
without thromboembolism, hemorrhage,
splenomegaly, or leukocytosis. Causes of secondary
thrombocytosis include chronic inflammatory
disorders (e.g., rheumatoid arthritis),
acute inflammatory disease, acute or chronic
blood loss, and malignancy. Recovery from
thrombocytopenia (“rebound”) can also result
in very high platelets. A common cause is withdrawal
from alcohol. (Lichtman, pp. 1786–1787)