d.

Parenchymatous degeneration of liver

Cellular swelling occurs because of marked mitochondrial damage, cessation of ATP production and
failure of sodium pump leading to increased osmotic pressure within cells. The alteration is on selective
permeability of cellular membranes leading to influx of water molecules.
PATHOGENESIS:
Acute cell swelling or hydropic degeneration occurs due to failure of the injured cells to maintain
electrolyte balance through the "Sodium-Potassium pump". As this mechanism is energy dependent, a
fall in ATP in injured cells causes the efflux of Potassium ions. With the influx of Sodium ions, the
increasing osmotic pressure in the cytoplasm attracts water molecules. As a result, swelling of the cells
occur, and is evident grossly as an enlarged pale and heavy organ. Microscopically, affected cells show
vacuoles in the cytoplasm with no distinct borders. The cytoplasm is diluted, and dispersed. This type of
degeneration is apt to be present in most types of injury. It is particularly severe in toxic and febrile
conditions. The condition is best seen in organs with intense metabolic rates of metabolism such as the
liver, kidneys, and brain.
MACROSCOPIC APPEARANCE:
In cellular swelling, at gross examination, the affected organ is enlarged, pale and soft.
MICROSCOPIC APPEARANCE:
Microscopically, the cells are enlarged, with a clear cytoplasm (due to the presence of small clear or
pale vacuoles, with indistinct shape and limits) and a normal nucleus in central position; blood
capillaries are compressed, explaining the organ's pallor.
e. Parenchymatous and fatty degeneration of liver
Fatty liver or steatosis hepatitis is present if the moist mass of the liver contains >10% fat, or if more
than 50% of the hepatic cells display medium or large-sized lipid vacuoles and there is a diffuse pattern
of distribution.
PATHOGENESIS:
The causes of the underlying fatty change may be:
Exogenous:
Increased fat transport
Increased carbohydrate intake
Endogenous:
Increased peripheral mobilization of fat
Inhibited intracellular utilization of fat in the hepatic cells

Increased fat synthesis in the hepatic cells

Decreased removal of fat
MACROSCOPIC APPEARANCE:
mild hepatomegaly (in ~75%)
attenuation/signal of liver shifted towards that of fat
focal fatty sparing
islands of normal liver tissue within sea of hepatic steatosis
MICROSCOPIC APPEARANCE:
At the beginning, the hepatocytes present small fat vacuoles in the vicinity of the endoplasmic
reticulum (liposomes) - microvesicular fatty change (photo). In the late stages, the size of the vacuoles
increases pushing the nucleus to the periphery of the cell - macrovesicular fatty change. These vesicles
are well delineated and optically "empty" because fat solves during tissue processing (paraffin
embedding). Large vacuoles may coalesce, producing fatty cysts - which are irreversible lesions.
f. Hemorrhagic infarct of lung
Hemorrhagic infarcts, also called red infarcts are bloody because venous or arterial obstruction occurs
in loose, spongy tissue or tissue with a dual blood supply, notably the lung (which has blood supply
from the right ventricle through the pulmonary artery and from the left ventricle via the bronchial artery
branches from the aorta). In these organs, occlusion of one area can cause infarction, but the other
supply continues to pump blood into the dead tissue.
PATHOGENESIS:
If emboli are small, they may pass through the main pulmonary arteries and become impacted in the
peripheral branches, usually in the arteries supplying the lower lobes of the lungs. Smaller emboli
impede the flow of blood through the lungs and raise pulmonary artery pressure, but they have a les
devastating effect than large emboli. Frequently, the segment of lung supplied by the obstructed
pulmonary artery undergoes necrosis, resulting in a pulmonary infarct. The alveolar septa break down,
and blood flows from the ruptured capillaries into the pulmonary alveoli which become distended with
blood.

MACROSCOPIC APPEARANCE:
These infarcts are haemorrhagic (dark brown to black in colour) and the
surrounding pulmonary parenchyma is consolidated. Compare this
parenchyma with that of the upper lobe which is normal. This
consolidation will be a result of the inflammatory response to the infarcts.
In areas of consolidation the alveolar air spaces appear more prominent
because they are clearly outlined by edematous inter-alveolar septae.

MICROSCOPIC APPEARANCE::
Histologically, the hemorrhagic area shows ischemic
necrosis of the alveolar walls, bronchioles and vessels. If
the infarct is caused by an infected embolus, the
neurtrophilic inflammatory reaction can be intense. Such
lesions are referred to as septic infarcts, some which turn
into abscesses.
They appear eosinophilic (pink), homogenous, lacking the
nuclei, but keep their shapes - "structured necrosis".
Alveolar lumens from infarcted area are invaded by red
blood cells

REFERENCES:
The Nature of Disease: Pathology for the Health Professions By Thomas H. McConnell
Essentials of Human Disease By Leonard V. Crowley
Robbins & Cotran Pathologic Basis of Disease By Vinay Kumar, Abul K. Abbas, Jon C. Aster
http://www2.mozcom.com/~emcdvm/path01.html
http://www.pathologyatlas.ro/cellular-swelling-liver.php
http://www.pathologyatlas.ro/fatty-change-liver-steatosis-pathology.php
http://radiopaedia.org/articles/diffuse-hepatic-steatosis
http://www.pathologyatlas.ro/hemorrhagic-infarct-lung-pulmonary-pathology.php
https://secure.health.utas.edu.au/intranet/cds/pathprac/Files/Cases/Respiratory/Case33/Case33.htm

RESEARCHER: brainiac