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32 Cards in this Set

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Name types of hyperplasia
Hormonal Hyperplasia (female brease glandular epithelium at puberty/pregnancy) and Compensatory Hyperplasia(liver restoration following resection)

Pathologic Hyperplasia: result of excessive hormonal stimulus. Ex: endometrial hyperplasia resulting from estrogen/progesterone imbalance(favoring estrogen). If balance restored, hyperplasia stops, unlike in neoplasia in which hyperplasia continues despite lack of stimulus.
Mechanisms leading to hyperplasia
Increase in GF, increase in GF receptors, Activation of particular intracellular signaling pathways
Causes of hypertrophy
Increased functional demand(skeletal muscles), Increased hormonal stimulus(pregnancy),
Causes of atrophy
Decreased workload, loss of innervation, decreased blood supply, inadequate nutrition, loss of endocrine stimulation, aging(senile atrophy of brain), pressure(compression due to tumor)
Name the enzyme responsible for degradation in lysosomes
Cathepsin, along with other acid hydrolases
Squamous Metaplasia
Columnar Respiratory Epithelium becomes squamous when exposed to excessive smoke.
Columnar Ductal Epithelium becomes squamous when ducts are obstructed.
Vitamin A deficiency causes many columnar epithelia to become squamous.
Columnar Metaplasia
Barrett's Esophagus -- the squamous epithelium of esophagus becomes columnar.
Connective Tissue Metaplasia
Cartilage, bone or fat emerge in tissues that do not normally contain these.
Myositis Ossificans, heterotopic bone formation in soft tissue
Necrosis vs Apoptosis
Necrosis has cell swelling, RANDOM breakdown of DNA, and protein denaturation.
Apoptosis has cell shrinkage, ORDERED breakdown of DNA, and formation of apoptotic bodies.
Karyolysis, Pyknosis, Karyorrhexis
Karyolysis is a fading of the basophilia of the nucleus
Pyknosis is a shrinkage and increased basophilia of nuclei
karyorrhexis is a fragmentation of a pyknotic nucleus
Discuss means of cell injury via reduced ATPty
when ATP falls bellow 10%, Na/K pump fails and Na enters cell followed by water causing swelling. Glycolytic increase reduced glucose levels and increases pH. Ca pump also fails leading to increase intracellular Ca which activates enzymatic destruction. Ribosomes detach from RER. Proteins misfold.
Mitochondrial Damage
Caused by influx of calcium, oxidative stress and phospholipid breakdown. Creates Mitochondrial Permeability Transition which leaks cytochrome C triggering apoptosis.
Name the locations of the important antioxidants present in the cell
Mitochondria: Superoxide Dismutase, Glutathione Peroxidase

Cytosol: SOD, Glutathione Peroxidase, Ceruloplasmin, ferritin, vitamin C

Membranes; Vitamin C, Vitamin E, Beta Carotene
Review Gangrenous Necrosis
Dry Gangrenous Necrosis is pretty much coagulative necrosis whereas wet gangrenous necrosis is necrosis that has turned liquefactive due to secondary infection
These indicate reversible cellular injury
Formation of blebs, loss of microvilli, detachment of ribosomes from RER, dysfunction of Na/K pump leading to cell swelling, glycolysis which decreases pH leading to nuclear clumping, formation of myelin figures
This indicates irreversible cell injury
Accumulation of amorphous calcium rich densities in mitochondrial matrix, mitochondrial vacuolization, loss of membrane integrity.
Discuss two pathways of apoptosis
The mitochondrial or intrinsic pathway which is dependent on Bcl-2 sensor proteins. Lack of survival factors, radiation or other stress can set this reaction off.

The death receptor pathway works by a TNF receptor called Fas. Fas Ligand on T-cells attack to the Fas receptor and active caspases to initiate apoptosis.
What does the Smooth ER do?
It is responsible for metabolizing barbiturates.
Name the cytoskeletal components
Microtubules, Thick myosin filaments, Intermediate filaments and thin actin filaments

Intermediate filaments: keratin(epithelial cells), neurofilaments(neurons, desmin filaments(muscle), vimentin filaments(connective tissue), glial filaments(astrocytes)
Causes of lipid accumulation in cells
Alcohol, Carbon Tetrachloride, Anoxia and starvation
What can you use to stain lipids?
Oil Red O and Sudan IV stains lipid orange-red and will not stain water or glycogen.

Note: Fat is dissolved in routine tissue processing so stains must be applied on fresh samples.
What does Periodic Acid-Schiff stain?(PAS)
It stains glycogen bright pink but will not stain fat or water. Glycogen will dissolve if processed with diastase.
Discuss cardiac steatosis.
Cardiac steatosis is caused by Hypoxia. Moderate hypoxia causes the tigered effect made by alteration of normal/lipid myocardium. profound hypoxia will just make a diffuse yellow coloration all around heart.
Discuss cholesterol accumulations
occurs in Atherosclerosis where macrophages(foam cells) and smooth muscle become laden with lipid vacuoles.
Cholesterol that leaks into extracellular space will crystallize.

Xanthomas are accumulations of foamy macrophages that are present on dermis and tendons.

Niemann Pick disease type C allows cholesterol build up in many organs.

Myelin figures present in necrosis are composed of lipids.
What is a Russell Body?
expanded ER as a result of chronic inflammation
Alpha 1 Antitrypsin Deficiency
abnormal alpha 1 antitrypsin due to misfolding builds up and destroys liver. Also causes emphysema
Familial hypercholesterolemia
mutations in LDL interfere with proper folding
describe Carbon pigment
It is black and is the most common exogenous pigment
describe lipofuscin pigment
It is the wear and tear pigment that accumulates with aging. It is brown and intracytoplasmic. Most prominent in liver and heart of elderly/malnourished.
Most commonly seen brown-black endogenous pigment.
golden-yellow to brown pigment formed from breakdown of hemoglobin and represents major storage for form of iron.

Prussian Blue stain is used to identify hemosiderin. It stains intensely blue.

Widespread hemosiderin deposits are present in hereditary hemochromatosis and hemosiderosis.
non-iron containing pigment in bile that stains yellow-green.