Download Kribriformní adenokarcinom jazyka

Cell injury:necrosis, apoptosis.
Adaptations:atrophy,
hypertrophy,hyperplasia.
Metaplasia.
2011
DEFINITIONS OF BASIC ASPECTS
OF DISEASE PROCESS





epidemiology (occurrence and incidence of
d.)
etiology (causes of disease)
pathogenesis (mechanisms of disease)
morphology of the tissue changes
clinical significance and consequences
classification of diseases


congenital- present at birth, even though
they are sometimes recognized later
acquired- occur only later after births
(infectious, nutritional, chemical, physical,
radiation injury etc.)
CELL INJURY


Causes of cell injury heterogeneous, range from gross
mechanical external causes to mild endogenous causes
as genetic lack of enzymes etc.
Normal cell is confined to relatively narrow range of
functions and structure by its genetic program to handle
normal physiologic demands


homeostastatic „steady„ state
Cells react to adverse influence by



adapting
sustaining reversible injury
suffering irreversible cellular injury- cell death
cellular adaptation


More excessive stimuli (either physiologic or pathologic)
 Cellular adaptation
 altered steady state
excessive work stress causes the increase in muscle mass that
reflects the increase in size of the individual muscle fiber - higher
level of metabolic activity -new equilibrium


adaptive response, in which there is a decrease in the size and
function of the cells


hypertrophy
vascular atrophy- results from slow long-lasting decrease of blood
supply
If the limits of adaptive mechanisms are exceeded or
when no adaptive response is possible- cell injury
Cell injury


Reversible cell injury denotes pathologic
changes that can be reversed when the
stimulus is removed and the cellular injury has
been mild. Cell injury is reversible- up to
certain point.
Irreversible cell injury denotes pathologic
changes that are permanent and cause cell
death, cannot be reversed to normal state
Cell death
Cell death
Cell death
Necrosis



defined as the morphologic changes that
following the cell death in a living tissue or
organ resulting from the progressive
degradative activity of catalytic enzymes on
lethally injured cells
These enzymes are derived either from dying
cells themselves-autolysis
or from lysosomal enzymes of leukocytes heterolysis
COAGULATIVE NECROSIS



most common pattern
hypoxic death- results from sudden severe
ischemia
Coagulative necrosis implies preservation of the
basic outline of coagulated cells for several days


nucleus usually disappears, but the shape of cell is
preserved
best example of coagulative necrosismyocardial infarction
Coagulative necrosis
Myocardial infarct
Histological hallmarks of myocardial infarction:
Thin, wavy and hypereosinophilic cardiomyocytes lacking nuclei and
inflammatory infiltration of the interstitium
Coagulative necrosis
Kidney infarct
Necrotic
tissue
Viable
tissue
necrosis
Demarcation line
Coagulative necrosis
Infarct of the spleen
LIQUEFACTIVE NECROSIS

results from rapid action of hydrolytic enzymes



characteristic of ischemic necrosis of brain, pancreas
also common in bacterial lesions


autolysis and heterolysis prevail over denaturation of proteins
-due to activity of enzymes of bacterial and leukocytic origin
good example of liquefactive necrosis is brain infarction
gross morphology



very soft and fluidly, tissue liquefaction
results in subsequent pseudocystic degeneration
no fibrous scar is formed, necrotic area changes into
postmalatic pseudocyst (postnecrotic)
Liquefactive necrosis
Encephalomalacia
(liquefactive necrosis of
the brain) and the
resulting postmalatic
pseudocyst
FAT NECROSIS
due to action of activated lipases
acute pancreatic necrosis,




in which active pancreatic enzymes cause focal necrosis of the
pancreas and the adipose tissue throughout the abdomen
lipases are activated and released and destroy not only
pancreatic tissue itself but also fat cells in the pancreas and
also fat cells throughout the peritoneal cavity
Balser necrosis


sharply circumscribed foci of enzymatic necroses of fat tissue
with shadowy outlines surrounded by a zone of inflammation
Liquefactive necrosis
So-called Balser´s necrosis of pancreatic and peripancreatic fat
Shadows of dead fat cell that have
undergone enzymatic necrosis
Viable pancreatic
glandular tissue
CASEOUS NECROSIS
in tuberculosis
Gross morphology





it appears grossly as soft, friable, whitish-gray
debris resembling cheesy material -caseous necrosis
Histologically, caseous necrosis appears as
amorphous eosinophilic material with cell debris
specific granulomatous inflammatory reaction



Composed of epithelioid histiocytes
giant cells of Langhans type
lymphocytes
Caseous necrosis
Yellow „cheesy“ areas of caseous necrosis in TBC lymphadenitis
GANGRENOUS NECROSIS



dry gangrene- black and dry and is sharply demarcated from
viable tissue

in extremities as a result of ischemic coagulative necrosis doe
to arterial obstruction
wet gangrene- results from severe bacterial infection

extremities due to arterial obstruction,

in acute suppurative appendicitis

tissue is swollen, reddish-black with extensive liquefaction

wet gangrene is severe complication associated with high
mortality rate
gas gangrene- is a wound infection caused by Clostridium
perfringens

extensive necrosis, tissue destruction, and production of gas by
fermentative action of bacteria

presence of gas in tissues -crepitus

associated with a high mortality rate
Healing of necrosis
regeneration
necrosis
scar
postnecrotic
pseudocyst
Cellular adaptation and repair
Atrophy

Reduction in size of a previously normal
organ
As opposed to:



Hypoplasia: insufficient growth of the organ during its
development
Aplasia: inborn lack of the organ
Agenesis: inborn lack of the primordium of the organ
Atrophy






under pathologic conditions-pathologic adaptation
There are four main adaptive states:
atrophy- shrinkage of the organ as a result of decreased
cell size or/and the cell number
hypertrophy - enlargement of the organ as a result of
increased cell size
hyperplasia - enlargement of the organ as a result of
increased cell number
metaplasia -the replacement of one cell type by another
cell type in a tissue or organ
Vascular atrophy of the kidney
is caused by a long standing gradual incomplete narrowing of the renal artery
Brown atrophy of the liver
is an example of senile atrophy
Aging
Diminution of cells
Accumulation
of lipofuscin
in cells due to its
poor solubility
during their aging
Brown atrophy
Hydronephrosis
is an example of mechanical atrophy due to compression of the renal parenchyma by
dilated pelvis (e. g. in the setting of urolithiasis)
Normal kidney
Dilated calyces in
moderate
hydronephrosis
Severe hydronephrosis
Renal
parenchyma
Flattened
papilla
Dilated calyx
Histological hallmark of hydronephrosis is flattening of the renal papilla. On higher
power you can see glomerular and tubular atrophy
Hypertrophy and hyperplasia


Hypertrophy: enlargement of an organ
due to enlargement of its cells
Hyperplasia: enlargement of an organ
due to increase in number of cells
Normal
Hypertrophy
Myocardial hypertrophy
is characterized by increased thickness of cardiac walls and
increased weight of the heart
Myocardial hypertrophy
Normal myocardium

Enlargement of prostate may be due to:
Hyperplasia
 Adenocarcinoma

Hyperplasia

Adenocarcinoma

Hyperplasia

Adenocarcinoma
Imunohistochemical staining for HMW cytokeratin 34βE12

Hyperplasia

Adenocarcinoma
+ orchiectomy?
TURP
Metaplasia
Reversible change in which one adult
cell type is replaced by another adult
Other possible but
cell type
usually not used
differentiation lines
Injury
Normal line of
differentiation
Stem cell
New line of
differentiation
Stem cell
Metaplasia


is an abnormality of cell differentiation in which one type of mature
cell is replaced by a different type of adult cell
squamous metaplasia n



glandular metaplasia





nonsquamous columnar or pseudostratified epithelium is replaced by
stratified squamous epithelium
in uterine cervix, in bronchial mucosa, in nasal cavity and paranasal
sinuses
occurs in the oesophagus, where the normal epithelium is replaced by
glandular mucus secreting epithelium Barret oesophagus
Clinical significance: risk of development of peptic ulcer in metaplastic
gastric mucosa
intestinal metaplasia - occurs often in chronic gastritis
Metaplasia only rarely occurs in mesenchymal tissue:
osseous metaplasia - in scars