CELLULAR RESPONSES TO STRESS Flashcards
Increase in SIZE of cells resulting in increased size of organ; cellular adaptation of non-dividing cells e.g. myocardial fibers
HYPERTROPHY
Increase in NUMBER of cells
HYPERPLASIA
REDUCTION in cell SIZE and NUMBER resulting in decreased size of organ
ATROPHY
A REVERSIBLE change wherein one differentiated cell type is replaced by another cell type
METAPLASIA
55/M, with long-standing history of hypertension, eventually expired from myocardial infarction. Autopsy: increased thickness of the left ventricular wall with large areas of fibrotic scars. What is the diagnosis, and what cellular adaptation is seen in this case?
Myocardial infarction; Left ventricular hypertrophy; Pathologic hypertrophy
47 G0, with granulosa cell tumor, presented with menorrhagia. UTZ showed thickened endometrium. Patient underwent diagnostic curettage. Biopsy shows back-to-back endometrial glands with nuclear atypia. What is the diagnosis (for the endometrium), and what cellular adaptation is seen in this case?
Complex atypical hyperplasia; Pathologic hyperplasia
35/M, with history of poliomyelitis, presented with disproportionately thinner right lower extremity. Muscle Biopsy shows decrease in size of skeletal myocytes. What is the cellular adaptation seen in this case?
Denervation atrophy; Pathologic atrophy
35/M, with history of poliomyelitis, presented with disproportionately thinner right lower extremity. Muscle Biopsy shows decrease in size of skeletal myocytes. What is the cellular adaptation seen in this case?
DENERVATION ATROPHY; PATHOLOGIC ATROPHY
39/F, with long-standing history of heartburn and water brash. Endoscopy showed multiple pinkish-tan areas at the GEJ. Biopsy shows fragments with simple columnar epithelium with goblet cells. What is the diagnosis, and what specific cellular adaptation is seen in this case?
Barrett esophagus; Intestinal metaplasia
The first manifestation of almost all forms of injury to cells; change is due to influx of ions (and consequently, water) due to failure of energydependent ion pumps (Na + -K + -ATPase)
CELLULAR SWELLING
Appearance of lipid vacuoles in the cytoplasm; often seen in cells participating in fat metabolism (liver, heart)
STEATOSIS
enlarged (swelling)
A. NECROSIS
B. APOPTOSIS
A.
pyknosis -> karyorrhexis -> karyolysis
A. NECROSIS
B. APOPTOSIS
A.
disrupted plasma membrane
A. NECROSIS
B. APOPTOSIS
A.
reduced (shrinkage)
A. NECROSIS
B. APOPTOSIS
B.
fragmentation into nucleosome-sized fragments
A. NECROSIS
B. APOPTOSIS
B.
intact plasma membrane
altered structure especially orientation of lipids
A. NECROSIS
B. APOPTOSIS
B.
Intact cellular contents; maybe released in apoptotic bodies
A. NECROSIS
B. APOPTOSIS
B.
No adjacent inflammation
A. NECROSIS
B. APOPTOSIS
B.
often physiologic; may be pathologic
A. NECROSIS
B. APOPTOSIS
B.
Enzymatic digestion; cellular contents leak out of cell
A. NECROSIS
B. APOPTOSIS
A. NECROSIS
frequent adjacent inflammation
A. NECROSIS
B. APOPTOSIS
A.
Invariably pathologic
A. NECROSIS
B. APOPTOSIS
A.
a form of necrosis wherein component cells are dead but the basic tissue architecture is PRESERVED
Coagulative necrosis
Digestion of dead cells, resulting in transformation of the tissue into a viscous liquid mass
Liquefactive necrosis
The term reserved for ischemic coagulative necrosis of the limbs (dry); may have superimposed bacterial infection with liquefactive necrosis (wet)
Gangrenous necrosis
Cheese-like gross appearance of necrotic areas; often seen in tuberculous infections; tissue architecture is NOT PRESERVED
Caseous necrosis
Focal areas of fat destruction, typically seen in acute pancreatitis; foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits (saponification), surrounded by an inflammatory reaction
Enzymatic fat necrosis
Cheese-like gross appearance of necrotic areas; often seen in tuberculous infections; tissue architecture is NOT PRESERVED
caseous necrosis
typically seen in acute pancreatitis; foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits (saponification), surrounded by an inflammatory reaction
Enzymatic fat necrosis
Seen in immune reactions involving blood vessels; deposits of immune complexes, together with fibrin that have leaked out of vessels, result in a bright pink and amorphous appearance
fibrinoid necrosis
acidophilic tombstone
coagulative necrosis
types of apoptosis
initator pathways
intrinsic pathway
extrinsic pathway
mitochondrial pathway
apoptosis
intrinsic (mitochondrial) pathway
death receptor pathway
extrinsic receptor pathway
form of necrosis seen in ischemic injury to most solid organs (heart, spleen, kidney)
coagulative necrosis
form of necrosis from hypoxic death of cells within the CNS
liquefactive necrosis
Inactivation of anti-apoptotic BCL2 protein that leads to activation of BAX/BAK channel, allowing cytochrome c to leak out of the mitochondria, activating apoptosis
Intrinsic (mitochondrial) pathway
Activation of “death receptors” by appropriate ligands that leads to activation of apoptosis
Extrinsic (Death receptor) pathway
Calcium deposition occurring in dead tissues, in the absence of calcium metabolic derangements
Dystrophic calcification
Calcium deposition in normal tissues occurring in the setting of hypercalcemia; example: Calcinosis
Metastatic calcification
