Cell Adaption and Injury Flashcards
Hyperplasia
Increase in the number of cells in an organ/tissue
Hypertrophy
An increase in the size of individual cells
Atophy
decrease in cell size
Metaplasia
One adult cell type is replaced by another adult cell type
Hyaline Change
This is a descriptive term→ a glassy, pink appearance seen in H&E staining
necrosis
form of cell death that is associated with damage from an external source that overwhelms the cell’s ability to survive
anthracosis
inhaled and phagocytosed by macrophages in the alveoli; black
caspase
are a family of protease enzymes playing essential roles in programmed cell death and inflammation
nuclear pyknosis
small,dark chromatin. Due to chromtin condensation and cleavage.
Coagulative necrosis
dead tissue is preserved for a few days
Associated with ischemia
liquefactive necrosis
dead cells are completely digested, leaving only viscous liquid; Associated with bacterial and fungal infections and hypoxic tissue
Caseous necrosis
“cheesy” granular material
Associated with tuberculous infection
Fat necrosis
areas of fat destruction in which fatty acids products combine with calcium to produce chalky-white areas;
Associated with pancreatitis and leakage of pancreatic lipase into adjacent tissues
Dystrophic calcification
deposition of calcium salts in dying tissue
karyolysis
fading of chromatin
karyorrhexis
chromatin fragmentation
Metastatic calcification
occurs when there is increase serum calcium, and often happens in otherwise normal tissue
Proliferation of glandular breast tissue and endometrial growth occurring as a result of excessive estrogen stimulations are examples of what?
hyperplasia
muscle growth due to weight lifting and growth of the heart as a result of chronic hypertension is an example of what?
hypertrophy
Cell Adaption
Occurs as a result of chronic stimulation by relatively low level stress
Where does steatosis usually occur and what does it look like histologically?
Common in liver (alcohol damage)
Appears as round, clear spaces in the cytoplasm
What does atherosclerosis look like?
internally: cholesterol gives a foamy appearance
Extracellularly: cholesterol molecules tend to crystallize and appear as shard-like
Describe amyloidosis
Amyloid are small, non-branching fibrils that physically resemble one another
These proteins fold abnormally and are associated with deposition which can lead to pressure atrophy of adjacent cells
Common histologic appearance: hyaline
Stained using Congo Red Stain
What causes hyaline change?
intracellular or extracellular accumulations of proteins
Glycogen generally accumulates in what kind of patients and what does it look like?
May accumulate in patient with abnormalities in glycogen or glucose metabolism (DM II)
Generally appear as clear, cytoplasmic vacuoles in H &E staining
Lipofuscin
a brown-yellow pigment that results from an incomplete breakdown of old subcellualr components; “wear and tear pigment”; commonly seen in the heart and liver of aging patients
Hemosiderin
a golden yellow-brown pigment that is the result of blood breakdown with iron
Bilirubin
a yellow pigment derived from blood breakdown with no iron
What are the major causes of cell injury?
Hypoxia Physical agents chemical agents/ drugs infection immunologic reactions and derangements genetic derangements nutritional deficiencies and imbalances
What are the 4 major targets of cell injury?
biochemical machinery for aerobic respiration (ATP production)
integrity of cell membranes
protein synthesis
integrity of the genetic apparatus of the cell
Depletion of ATP leads to what 5 things?
1) cell swelling ( Na/K pump)
2) decease in pH (LA)
3) abnormal protein folding
4) decrease in protein synthesis
4) increase in Ca++
What 3 things cause mitochondrial damage?
increase in Ca++, ROS, and oxygen deprivation
What 3 consequences result as a result of Ca++ influx?
1) opening of the mitochondrial permeability transition pore (cyt c)
2) activation of numerous enzymes (ases)
3) direct activation of caspases, inducing apoptosis
What are the principal free radicals?
OH
O2
H2O2
ONOO
What are the 3 main consequences of free radicals in cell injury?
1) lipid peroxidation and membrane damage
2) oxidative modification of proteins–> protein damage
3) lesions in DNA
What are the 5 sources of free radicals?
1) by products of mitochondrial oxidative phosphorylation
2) leukocytes (inflammation)
3) metals (Fe and copper)
4) radiant energy
5) NO
What 3 agents remove free radicals?
1) antioxidants
2) transfer proteins (transferrin, ferritin, ceruloplasmin)
3) enzymes
Describe the 4 major steps to apoptotic cell death?
1) cell shrinkage and increased density of cytoplasm
2) Nuclear pyknosis
3) cytoplasmic blebs
4) apoptotic bodies
Describe the mophological signs of reversible injury?
EM 1) plasma blebbing and loss of microvilli 2) mitochondrial swelling 3) dilation of endoplasmic reticulum LM 1) cellular swelling 2) fatty change
Describe the signs of irreversible injury
EM 1) membrane discontinuity 2) marked swelling of mitochondria 3) myelin figures LM 1 ) cytoplasmic eosinophilia (dark pink cytoplasm) 2) calcification of fatty acids 3) nuclear changes--> karyolysis, pyknosis, karyorrhexis (chromatin fragmentation) and loss of nucleus
Which necrosis is associated with ischemia?
coagulative
Which necrosis is associated with bacterial and fungal infections?
fungal/bacterial
Which type of necrosis is associated with TB?
caseous
which necrosis is associated with pancreatitis and leakage of pancreatic lipases?
fat necrosis
