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Ficat

1. Chist hidatic
Anatomie Patologica
• Macroscopic – unilocular/multilocular(T. E. Multilocularis)
- unic(75 %)/multiplu(25%)
- cu afectare izolat hepatica/afectare complexa(ficat+alte organe)
• 85 % din chistele hidatice hepatice afecteaza lobul drept hepatic
• Structura Chistului Hidatic Hepatic( int spre ext):
• Lichidul Hidatic lichid steril, opalescent sau limpede, alcalin si puternic
antigenic (reactii alergice!!); contine “nisipul hidatic” care reprezinta partea
fertila a chistului format de scolecsii invaginati precum si veziculele fiice sau
proligere (chiste hidatice “in miniatura”);
• Membrana proligera (germinativa) este responsabila de producerea efectiva
a chistului hidatic. - spre interior secreta lichidul hidatic;
- spre exterior secreta cuticula
- poate “inmuguri” atit la interior cind produce “vezicule fiice” cit si la
exterior cind produce chiste hidatice conexe
Cuticula sau adventicea reprezinta membrana proprie externa a chistului
hidatic( lame concentrice de material amorf), impermeabila pentru microbi si
albumine dar permite trecera prin osmoza a coloidelor si cristaloidelor intr-
un sens si a
toxinelot chistului in sens opus.
• Perichistul (sau ectochistul) reprezinta stratul extern al chistului hidatic
hepatic, este specific acestei localizari si este produs din tesutul hepatic al
gazdei prin presiunea cresterii in volum al chistului si prin reactii alergice
date de prezenta chistului.
• Chistul hidatic alveolar (multilocular) nu prezinta capsula (cuticula)
=>caracter mai invaziv (interventia chirurgicala este mai dificila tehnic).

Differential Diagnoses
Cystic Teratoma
Liver Abscess
Pyogenic Hepatic Abscesses
2. Meningita bacteriana

Microscopic: hiperemie meningeala, edem inflamator, infiltratete


granulocitare perivasculare sau difuze in panza, eventual continuate in
profunzime de-a lungul tecilor.

3. Pancreatita necrotica

Microscopie
a) Clasificate ca tipuri de hemoragie acută interstițială sau acută
b) Interstițiu acut: de obicei, un infiltrat de celule inflamatorii
acute, amestecat cu edem și exudat fibrinos
c) Hemoragia acută: necroza pruriginoasă, de obicei, într-o
distribuție peridocală sau perilobulară, cu o reducere a porțiunilor
pancreasului; difuze edeme interstițiale datorate scurgerilor
microvasculare, necrozei grase, neutrofilelor, distrugerii acinare și a
vaselor sanguine, hemoragiei interstițiale
d) De asemenea, omogenizarea celulelor acinare, dilatarea ductală
cu metaplazie mucinoasă sau scuamoasă, fibroblaste, trombi în
capilare și venule
e) Inițial sunt prezente neutrofile, apoi macrofage și limfocite
ulterioare
f) Calcificarea are loc devreme și pe scară largă

4. Infarct miocardic
[ACUTE MYOCARDIAL INFARCTION]. Acute myocardial infarction (AMI) is the
consequence of sudden loss of blood supply to myocytes with resultant ischemic
necrosis. The histopathologic changes are similar to tissue necrosis at other sites but
specific histologic changes depend on stage of infarction. This photomicrograph
shows an area of infarct (top arrow) that is paler than the relatively viable area (right
arrowhead). This large area of infarct is about 3 day old.

[ACUTE MYOCARDIAL INFARCTION]. The histopathologic changes follow a predictable


sequence in time with coagulative necrosis as the earliest light microscopic finding identified
at 4-12 hours after infarction in surviving patients. The necrosis is followed by infiltration of
neutrophils seen at about 12-24 hours after onset of infarction. This photomicrograph shows
an area of infarction with edema and heavily infiltrated by neutrophils (top arrow). This
infracted area is sharply demarcated from relatively preserved myocardium (bottom
arrowhead).
[ACUTE MYOCARDIAL INFARCTION]. This photomicrograph shows a 3-day old acute
infarct with a heavy neutrophilic infiltrate (arrow). The necrotic myocytes are replaced by
collection of neutrophils to initiate the process of inflammation and repair.

[ACUTE MYOCARDIAL INFARCTION]. This higher magnification image shows damaged


myocytes (arrowheads) with dissolution of cellular bodies in areas of neutrophilic infiltrate
(arrow). The neutrophils release enzymes that help dissolve dead cell bodies which are to be
phagocytized by macrophages recruited in the next phase.
[ACUTE MYOCARDIAL INFARCTION]. This 5-day-old infarct shows dead myocytes
(arrows) surrounded by a mixture of neutrophils and macrophages. With progressive
inflammation the neutrophils begin to die and replaced by influx of macrophages. The
process of inflammation is intertwined by the process of repair.