Cellular Responses to Stress and Inflammation and Repair Flashcards
Increase in SIZE of the cells — increased size of organ
Cellular adaptation of NON DIVIDING CELLS - myocardial fibers
HYPERTROPHY
Increase in NUMBER of cells
HYPERPLASIA
REDUCTION in cell SIZE and NUMBER — decreased size of organ
ATROPHY
A REVERSIBLE change wherein one differentiated cell type is REPLACED by ANOTHER cell type
METAPLASIA
55/M
long standing HPN, expired from MI
autopsy showed INCREASED thickness of the L ventricular wall w/ large areas of fibrotic scars
diagnosis and cellular adaptation
Myocardial Infarction
Left Ventricular Hypertrophy
Pathologic HYPERTROPHY
47 G0 w/ granulosa cell tumor presented w/ menorrhagia
UTZ showed endometrium
Px underwent diagnostic curettage
Biopsy showed BACK TO BACK ENDOMETRIAL GLANDS w/ NUCLEAR ATYPIA
diagnosis and cellular adaptation
Complex Atypical Hyperplasia
Pathologic Hyperplasia
35/M w/ hx of poliomyelitis presented w/ disproportionately thinner R lower extremity
Muscle biopsy showed DECREASE in size of skeletal myocytes
cellular adaptation
Denervation Atrophy
Pathologic Atrophy
The FIRST MANIFESTATION of almost all forms of injury to the cells
Change is d.t. INFUX of IONS (and water) d.t. FAILURE of ENERGY DEPENDENT ION PUMPS (NaKATPase)
CELLULAR SWELLING
Appearance of LIPID VACUOLES in the CYTOPLASM
Often seen in cells participating in fat metabolism (LIVER, HEART)
Steatosis
Type of cell death that results from PATHOLOGIC cell injury
Necrosis
Type of cell death that is energy dependent tightly regulated and associated w/ normal cellular functions often physiologic
PROGRAMMED CELL DEATH
Apoptosis
Component cells are dead but the basic structure is PRESERVED (acidophilic tombstone)
ISCHEMIC INJURY to MOST SOLID ORGANS (heart, spleen, kidney) EXCEPT BRAIN
Coagulative Necrosis
Digestion of dead cells — transformation of the tissue into a VISCOUS LIQUID MASS
Often seen in INFECTION (PUS) and hypoxic death of cells w/n CNS
Liquefactive necrosis
The term reserved for ISCHEMIC COAGULATIVE NECROSIS of the LIMBS (dry)
May have superimposed bacterial infection w/ liquefactive necrosis (wet)
Gangrene necrosis
CHEESE LIKE gross appearance of necrotic areas
Often seen in TUBERCULOUS INFECTIOUS
Tissue architecture is NOT PRESERVED
Caseous necrosis
Focal areas of fat destruction seen in ACUTE PANCREATITIS
Foci of necrosis contain SHADOWY OUTLINES OF NECROTIC FAT CELLS with basophil calcium deposits (SAPONIFICATION) surrounded by INFLAMMATORY REACTION
Enzymatic Fat Necrosis
Seen in IMMUNE REACTIONS involving BLOOD VESSELS; deposits of immune complexes together w/ FIBRIN that have leaked out vessels — BRIGHT PINK and AMORPHOUS APPEARANCE
Fibrinoid 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 activation of apoptosis
Extrinsic (Death Receptor) Pathway
Calcium deposition occurring in DEAD TISSUES in the ABSENCE of CALCIUM METABOLIC DERANGEMENTS
i.e. Psammoma bodies (cancers w/ papillary architecture and meningioma)
Dystrophic Calcifications
Calcium deposition in NORMAL TISSUES occurring in the setting of HYPERCALCEMIA
i.e. Calcinosis
Metastatic Calcifications
ACUTE INFLAMMATION
fast; minutes or hrs
NEUTROPHILS
mild and self limited
prominent local and systemic signs
CHRONIC INFLAMMATION
slow, days
MONOCYTES/MACROPHAGES and LYMPHOCYTES
severe and progressive
less local and systemic signs
Components of Acute Inflammation
- DILATION of small vessels
- INCREASED microvascular PERMEABILITY
- EMIGRATION of leukocytes and their ACTIVATION
