Cell injury- reversible & irreversible Flashcards
(43 cards)
1
Q
Acute cell swelling
A
-hydropic degeneration; hydropic change; cytotoxic edema; ballooning degeneration
2
Q
What is highly vulnerable to hypoxia and cell swelling?
A
- cardiomyocytes
- proximal renal tubule epithelium
- hepatocytes
- endothelium
- CNS neurons, oligodendrocytes, astrocytes
3
Q
Definition of acute cell swelling
A
- early, sub-lethal manifestation of cell damage, characterized by increased cell size and volume due to H2O overload
- most common and fundamental expression of cell injury
4
Q
Etiology of acute swelling
A
- loss of ionic & fluid homeostasis
- failure of cell energy production
- cell membrane damage
- injury to enzymes regulating ion channels of membranes
ex. hypoxia, toxic agents
5
Q
Gross appearance of acute cell swelling
A
- slightly swollen organ w/ rounded edges
- pallor when compared to normal
- cut surface: tissue bulges & can not be easily put in correct apposition
- slightly heavy
6
Q
Example of ballooning degeneration resulting in formation of a
A
vesicle (bullae/blister)
7
Q
Histologic appearance of cellular swelling
A
- H2O uptake dilutes the cytoplasm
- cells are enlarged w/ pale cytoplasm
- may show increased cytoplasmic eosinophilia
- nucleus in normal position, w/ no morphological changes
8
Q
Ultrastructural changes of cellular swelling
A
- Plasma membrane alterations, such as blebbing, blunting, & loss of microvilli
- Mitochondrial changes, including swelling and the appearance of small amorphous densities
- Dilation of the ER, w/ detachment of plysomes; intracytoplasmic myelin figures may be present
- Nuclear alterations, w/ disaggregation of granular & fibrillar elements
9
Q
Hydropic change, fatty change (cell swelling)
A
-due to increase uptake of H2O & then to diffuse disintegration of organelles & cytoplasmic proteins
10
Q
Hypertrophy (cell enlargement)
A
-the cell enlargement is caused by increase of normal organelles
11
Q
Prognosis of cellular swelling
A
- depends on the # of cells affected & importance of cells
- Good (if O2 is restored before the “point of no return”)
- Poor (progression to irreversible cell injury)
12
Q
Definition of fatty change
A
- sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation
- may be preceded or accompanied by cell swelling
13
Q
All major classes of lipids can accumulate in cells:
A
- triglycerides
- cholesterol
- phospholipids
- abnormal complexes of lipids & carbs
14
Q
Lipidosis
A
- accumulation of triglycerides & other lipid metabolites (neutral fats & cholesterol) w/in parenchymal cells
- heart muscle
- skeletal muscle
- kidney
- liver
15
Q
Etiology of fatty change
A
- main causes: hypoxia, toxicity, metabolic disorders
- seen in abnormalities of synthesis, utilization &/or mobilization of fat
16
Q
Pathogensis of fatty change
A
- impaired metabolism of fatty acids
- accumulation of triglycerides
- formation of intracytoplasmic fat vacuoles
17
Q
Gross appearance of fatty change
A
- liver: diffuse yellow
- enhanced reticular pattern if specific zones of hepatocytes are affected
- edges are rounded & will bulge on section
- tissue is soft, often friable, cuts easily and has a greasy texture
- if condition is severe small liver sections may float in fixative or water
18
Q
Physiologic hepatic lipidosis
A
in late pregnancy (pregnancy toxemia) & heavy early lactation (ketosis) in ruminants
19
Q
Hepatic lipidosis nutritional disorders
A
- obesity
- proteins-calorie malnutrition
- starvation
20
Q
Hepatic lipidosis endocrine dz
A
- diabetes mellitus
- feline fatty liver syndrome, fat cow syndrome
21
Q
Histologic appearance of fatty change
A
- well delineated, lipid-filled vacuoles in the cytoplasm
- vacuoles are single to multiple either small or large
- vacuoles may displace the cell nucleus to the periphery
22
Q
Prognosis of fatty change
A
-initially reversible: can lead to hepatocyte death (irreversible)
23
Q
Hepatic lipidosis
A
is seen in cats, ruminants, camelids, and mini equines but is rare in dogs and uncommon in other horses
- more often in obese cats, secondary to anorexia of any cause
- mortality is high w/o tx
24
Q
Irreversible injury is associated morphologically with:
A
- severe swelling of mitochondria
- extensive damage to plasma membranes (giving rise to myelin figures)
- swelling of lysosomes
25
Cell death
- mainly by necrosis
| - apoptosis also contributes
26
Necrosis (AKA Oncosis, Oncotis necrosis)
-cell death after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury
27
Necrosis morphologic aspect is due to 2 concurrent processes:
-denaturation of proteins
-enzymatic digestion of the cell
(-by endogenous enzymes derived from the lysosomes of the dying cells=autolysis (self digestion))
(-by release of lysosomes content from infiltrating WBCs)
OUTCOME: INFLAMMATION
28
Necrosis Gross Appearance
-pale, soft, friable and sharply demarcated from viable tissue by a zone of inflammation
29
Cause of changes of necrotic cells in cytoplasm
- denatured proteins
- loss of RNA
- loss of glycogen particles
- enzyme-digested cytoplasm organelles
30
Appearance of changes of necrotic cells in cytoplasm
- increase binding of eosin (pink)
- loosing basophilia
- glassy homogeneous
- vacuolation and moth eaten appearance
- calcification may be seen
31
Pattern of tissue necrosis
- may provide clues about the underlying cause
| - do not reflect underlying mechanisms but are used by pathologists and clinicians
32
Coagulative (coagulation) necrosis
-architecture of dead tissues is preserved (days)
-ultimately the necrotic cells are removed:
~phagocytosis by WBCs
~digestion by the action of lysosomal enzymes of the WBCs
33
Common cause of Coagulative (coagulation) necrosis
Ischemia in all solid organs except the brain
34
Liquefactive necrosis
- necrotic architecture is liquefied = liquid
| - dead cells are "digested" --> transformation of the tissue into a liquid viscous mass
35
Liquefactive necrosis occurs in
-tissue with high neutrophil recruitment and enzymatic release w/ digestion of tissue
-tissues w/ high lipid content
-focal bacterial and occasionally, fungal infections
~microbes stimulate the accumulation of WBCs and the liberation of enzymes from these cells
36
Leukoencephalomalacia
| -pathogenesis
Ingestion of Fusarium moniliforme containing Fumonisin B1 Toxin-Producing Moldy Corn > Sphingolipid Synthesis Inhibition > Direct Cellular Toxicity > Leukoencephalomalacia
37
Leukoencephalomalacia
| -Species affected
-horse, also chicken, pig (pulmonary edema)
38
Leukoencephalomalacia necrosis of
white matter of cerebral hemispheres, brain stem and cerebellum
39
Necrotic material is frequently creamy yellow bc of the presence of dead WBCs
PUS
40
Abscess
a localized collection of pus (liquefied tissue) in a cavity formed by disintegration of tissues surrounded by fibrous connective tissue (not in CNS)
-bodies defensive rxn to foreign material
41
2 types of abscesses
-septic: (the majority)=infection, release of enzymes from WBCs and infectious agent
-Sterile: process caused by nonliving irritants such as drugs
~likely to turn into firm, solid lumps as they scar, rather than remaining pockets of pus
42
Histolgy of liquefactive necrosis
- loss of cellular detail
- cells are granular
- eosinophilic and basophilic debris
- neutrophil nuclei may dominate nuclear debris
- no tissue architecture is preserved
43
Gangrenous necrosis
not a specific pattern of celll death but begins mostly as coagulative necrosis
-likely due to ischemia
