Manar Hajeer, , MD, FRCPath th Unive vers rsity ity of Jordan an , school
- l of medicine
Manar Hajeer, , MD, FRCPath th Unive vers rsity ity of Jordan - - PowerPoint PPT Presentation
Manar Hajeer, , MD, FRCPath th Unive vers rsity ity of Jordan an , school ol of medicine cine If the damaging stimulus is removed >>>injured cells can return to normal Morpho pholo logy: gy: Cellular swelling
(1) plasma membrane alterations (blebbing,
(2) mitochondrial change (swelling and densities); (3) dilation of ER (4) nuclear clumping of chromatin. (5) Cytoplasmic myelin figures
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Increased cytoplasmic eosinophilia. Marked dilatation of ER , mitochondria. Mitochondrial densities. More myelin figures. Nuclear changes: Pyknosis: shrinkage and increased basophilia; Karyorrhexis :fragmentation; Karyolysis: basophilia fades
Different mechanisms,
Necro
Rapid and uncontrollable. Severe disturbances Ischemia, toxins, infections,
Apoptosis:
Less severe injury. Regulated by genes and
Controlled. Necro
Leakage of intracellular proteins through the damaged cell
Cardiac enzymes, liver enzymes.
Conserved tissue
Anuclear eosinophilic on LM Wedge shaped following
Leukocyte lysosomes and
Characteristic of all solid
Focal infections (pus) CNS infarcts Center liquefies and
Clinical term It is coagulative
Dry vs wet
“Cheese like” Combination of coagulative
Tissue architecture is not
Acellular center Usually enclosed in an
Most often seen in TB
Occurs in acute
Due to release of
Focal fat destruction Released FA’s combine
Visible by LM Deposits of antigen –
Seen in vasculitis