Intro To Pathology Lecture 2

Front 1

Name types of hyperplasia

Back 1

Physiologic:
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.

Front 2

Mechanisms leading to hyperplasia

Back 2

Increase in GF, increase in GF receptors, Activation of particular intracellular signaling pathways

Front 3

Causes of hypertrophy

Back 3

Increased functional demand(skeletal muscles), Increased hormonal stimulus(pregnancy),

Front 4

Causes of atrophy

Back 4

Decreased workload, loss of innervation, decreased blood supply, inadequate nutrition, loss of endocrine stimulation, aging(senile atrophy of brain), pressure(compression due to tumor)

Front 5

Name the enzyme responsible for degradation in lysosomes

Back 5

Cathepsin, along with other acid hydrolases

Front 6

Squamous Metaplasia

Back 6

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.

Front 7

Columnar Metaplasia

Back 7

Barrett's Esophagus -- the squamous epithelium of esophagus becomes columnar.

Front 8

Connective Tissue Metaplasia

Back 8

Cartilage, bone or fat emerge in tissues that do not normally contain these.
Myositis Ossificans, heterotopic bone formation in soft tissue

Front 9

Necrosis vs Apoptosis

Back 9

Necrosis has cell swelling, RANDOM breakdown of DNA, and protein denaturation.
Apoptosis has cell shrinkage, ORDERED breakdown of DNA, and formation of apoptotic bodies.

Front 10

Karyolysis, Pyknosis, Karyorrhexis

Back 10

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

Front 11

Discuss means of cell injury via reduced ATPty

Back 11

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.

Front 12

Mitochondrial Damage

Back 12

Caused by influx of calcium, oxidative stress and phospholipid breakdown. Creates Mitochondrial Permeability Transition which leaks cytochrome C triggering apoptosis.

Front 13

Name the locations of the important antioxidants present in the cell

Back 13

Mitochondria: Superoxide Dismutase, Glutathione Peroxidase

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

Membranes; Vitamin C, Vitamin E, Beta Carotene

Front 14

Review Gangrenous Necrosis

Back 14

Dry Gangrenous Necrosis is pretty much coagulative necrosis whereas wet gangrenous necrosis is necrosis that has turned liquefactive due to secondary infection

Front 15

These indicate reversible cellular injury

Back 15

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

Front 16

This indicates irreversible cell injury

Back 16

Accumulation of amorphous calcium rich densities in mitochondrial matrix, mitochondrial vacuolization, loss of membrane integrity.

Front 17

Discuss two pathways of apoptosis

Back 17

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.

Front 18

What does the Smooth ER do?

Back 18

It is responsible for metabolizing barbiturates.

Front 19

Name the cytoskeletal components

Back 19

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)

Front 20

Causes of lipid accumulation in cells

Back 20

Alcohol, Carbon Tetrachloride, Anoxia and starvation

Front 21

What can you use to stain lipids?

Back 21

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.

Front 22

What does Periodic Acid-Schiff stain?(PAS)

Back 22

It stains glycogen bright pink but will not stain fat or water. Glycogen will dissolve if processed with diastase.

Front 23

Discuss cardiac steatosis.

Back 23

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.

Front 24

Discuss cholesterol accumulations

Back 24

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.

Front 25

What is a Russell Body?

Back 25

expanded ER as a result of chronic inflammation

Front 26

Alpha 1 Antitrypsin Deficiency

Back 26

abnormal alpha 1 antitrypsin due to misfolding builds up and destroys liver. Also causes emphysema

Front 27

Familial hypercholesterolemia

Back 27

mutations in LDL interfere with proper folding

Front 28

describe Carbon pigment

Back 28

It is black and is the most common exogenous pigment

Front 29

describe lipofuscin pigment

Back 29

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.

Front 30

melanin

Back 30

Most commonly seen brown-black endogenous pigment.

Front 31

Hemosiderin

Back 31

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.

Front 32

Bilirubin

Back 32

non-iron containing pigment in bile that stains yellow-green.