Liver and Pancreas
Fig. 28.20 Hepatocellular carcinomas. Decreased reticulin fibers is
helpful in diagnosing hepatocellular carcinoma with minimal nuclear atypia.
Cell block (reticulin x MP).
Fig. 28.21 Fatty metamorphosis of the liver. Hepatocytes that contain
a single large, intracytoplasmic, clear vacuole or two or more small vacuoles.
Note that the large vacuoles displace the nuclei to the periphery of the cells
and distend the cells. FNA smear (Papanicolaou x HP).
and o th e r cytologic appearances are specific enough to be
detected b y lig h t microscopy.
A cc um u la tio n o f neutral triglycerides in hepatocytes is one o f
the m ost c om m o n pathologic changes in the liver. M a jo r causes
o f fa tty m etam orp hosis o f the liv e r include excess alcohol
intake, obesity, m a ln u tritio n , diabetes m ellitu s, and d e b ilitating
system ic diseases (e.g. leukem ias). Excess alcohol inta ke is by far
the m ost c om m o n cause o f fa tty liv e r in N o rth Am erica. Fatty
changes in alcoholics range fro m vac uo lation o f a fe w liv e r cells
to severe in vo lve m e n t o f the w h o le liver. In severe cases, the liv e r
is enlarged and liv e r fu n c tio n test results are m ild ly abnorm al.
The cytoplasm o f hepatocytes contains a single large clear vacu-
ole or, less frequently, m u ltip le sm all vacuoles o f variable sizes.
The large vacuoles displace the nuclei to the p erip hery o f the
cells and distend the cells (Fig. 28.21) . In the cases o f advanced
fa tty m etam orphosis, groupings o f liv e r cells w ith fa tty changes
m ay appear as sm all fragm ents o f adipose tissue in FN A smears.
T he presence o f occasional large ro u n d nuclei in som e cells
clearly distinguishes liv e r cell fragm ents fro m adipose tissue. It
is n o t possible to ascertain w h e th e r the fa tty m etam orp hosis is
due to a lcoholism o r to o the r causes on p urely c ytom orp holog ic
V ira l hep atitis is a necrotizing, inflam m ato ry, regenerative disease
o f liv e r parenchym al cells. E tiolog ically, type A, type B, type C,
type D, and type E v ira l hep atitis have been id entified ; however,
th ey cannot be re lia b ly distinguished fro m one a no the r o n cyto-
histo lo g ic grounds alone. Type A hep atitis is essentially a self-
lim ite d illness, and the chronic carrier state has n o t been show n
to exist. However, m ore th an 10% o f patients w ith hep atitis B
develop sig nificant sym ptom s, inc lu d in g acute fu lm in a n t illness
and various chronic disease states. The v ira l agents responsible
fo r type C and type D hep atitis also have the cap ab ility to
cause chronic hepatic disease. H ep atitis B virus and hep atitis C
in fe c tio n have been fo u n d to be a m a jo r risk factor in hepatic
carcinogenesis in the East and in N o rth Am erica, respectively. In
Taiw an, the incidence o f hep atocellular carcinom a in hep atitis B
surface antigen (H B sA g)-positive patients is 1158 per 100 000,
com pared w ith 5
per 100 000 in HbsAg-negative patients.
Reports fro m Taiw an showed th a t 80% o f patients w ith hepato-
cellular carcinom a have a chronic fo rm o f hep atitis B.
A c o m b in a tio n o f degenerative, inflam m ato ry, and regenerative
changes are seen. The degenerative changes are represented by
b a llo o n in g degeneration o f hepatocytes and isolated liv e r cell
necrosis in the fo rm o f a cid op h ilic bodies. T he affected hepa-
tocytes are enlarged and appear sw ollen, and th e ir cytoplasm is
lig h tly stained. The acid op h ilic bodies are degenerative hepato-
cytes th a t undergo shrinkage and karyopyknosis, w ith eventual
loss o f the nucleus. T he acid op hilic bodies in FN A preparations
prepared w ith Papanicolaou stain appear either b lu ish green o r
eosinop hilic. T he in fla m m a to ry changes in v ira l hepatitis include
m on on uc le a r in filtra te (m a in ly lym phocytes) and hyperplasia
o f K up ffer cells. K up ffer cells in noncohesive groupings m ay be
seen. The y often stain intensely w ith PAS after amylase diges-
tio n . The regenerative changes include p leo m o rp hism o f hepa-
tocytes, increased m ito tic activity, and an increase in the num b er
o f binucleated hepatocytes. These p leo m o rp hic hepatocytes,
u n lik e those seen in c irrho tic liver, m ay also undergo b a llo o n in g
degeneration generation. In som e cases, an increase in hem osi-
derin deposits is observed in K up ffer cells and hepatocytes.
E thyl alcohol is a liv e r to x in , and its effects on the liv e r depend
on the d u ra tio n and a m o u n t o f excess intake. T he essential
changes o f a lcoholic hep atitis are liv e r cell damage and in fla m -
m ation . Fibrosis is seen in later stages. Fatty change is usually