Pathology

Question 1

hypertophy definition and example

Answer 1

increased cell size; same cell number

E.g. Weightlifter muscles are larger than if they didn’t lift weights

[ὑπέρ (hupér, “over”); τροφή (trophḗ, “nourishment”]

Question 2

hyperplasia definition and example

Answer 2

increased cell number; +/- increased size

an adaptive response

E.g. Liver regeneration occurring after a portion is injured or removed is hyperplasia

[ὑπέρ (hupér, “over”); πλάσις (plásis, “formation”]

Question 3

atrophy definition and example

Answer 3

reduction in size d/t decrease in cell size and/or number

E.g. Uterus decreases in size in postpartum women after delivery; Brains are smaller in elderly compared to those in younger individuals

[ἀ- (a-, “not”); τροφή (trophḗ, “nourishment”)]

Question 4

metaplasia definition and example

Answer 4

one differentiated cell type is replaced by another; tissues will assume the phenotype that gives the best protection from the insult

E.g. Respiratory stratified columnar epithelium replaced by squamous metaplastic epithelium in smokers

[μετα (meta, “change”; πλάσις (plásis, “molding, formation”]

Question 5

reversible adaptations to stress as seen in tissue

Answer 5

hyperplasia
metaplasia
dysplasia
hypertrophy
atrophy

Question 6

dysplasia definition

Answer 6

lack of normal maturation which may become an invasive carcinoma

[δυσ- (dus-, “bad”); πλάσις (plásis, “formation”]

Question 7

hyperplasia causes

Answer 7

altered endocrine milieu, AKA hormonal stimulation (e.g. puberty)

increased functional demand (e.g. going to higher altitudes -> inc in erythropoietin lvls)

chronic injury (e.g. callus d/t repeated trauma)

Question 8

hyperplasia basic mechanism

Answer 8

stimulation of resting cells (Gₒ to G₁) and entry into cell cycle

Question 9

molecular mechanism of metaplasia

Answer 9

replacing the expression of one set of differentiation genes with another by reprogramming stem cells to differentiate along a new pathway

can become malignant over time and important normal protective mechanisms are lost

Question 10

dysplasia cause

Answer 10

response to persistent injury

Question 11

physiologic examples of atrophy during neonatal development

Answer 11

notochord (tail), which is present during the development of babies and goes away before birth

Question 12

causes of pathologic atrophy

Answer 12

decreased workload (disuse atrophy)

loss of innervation (denervation atrophy)

diminished blood supply (ischemic atrophy)

inadequate nutrition

loss of endocrine stimulation

pressure (pressure atrophy

Question 13

pressure atrophy

Answer 13

tissue compression for a length of time leads to atrophy of surrounding normal tissues

E.g. brain adjacent to a tumor; soft tissue over bone in bed ridden patients

Question 14

cachexia

Answer 14

muscle wasting

Question 15

disuse atrophy example

Answer 15

bed rest without using muscles leads to initial decrease in muscle fiber size (atrophy) and later decrease in number of muscle fibers (due to apoptosis) and decrease in muscle size (more atrophy)

Question 16

denervation atrophy

Answer 16

skeletal muscle fiber size and strength are dependent on nerves; with nerve injury, there will be denervation atrophy of the muscle supplied by the nerve

Question 17

ischemic atrophy

Answer 17

a gradual decrease in blood supply (atherosclerosis) leads to atrophy of supplied tissue (feet lose hair and skin appendages and skeletal muscle fibers); brain atrophies due to atherosclerotic vascular disease

Question 18

mechanism of atrophy

Answer 18

reduced metabolic activity -> decreased protein synthesis and increased degradation

cellular protein degradation follows the ubiquitin-proteasome pathway: nutrient deficiency and disuse may activate ubiquitin ligases which would target these proteins for degradation in proteasomes

may have an increase in autophagy: starved cell eats its own components in order to survive with reduced nutrient demand

Question 19

hypertrophy causes

Answer 19

Occurs in cells with terminal differentiation and relative inability for mitoses (skeletal muscle, cardiac muscle) and in cells that can divide as well as increase in size (liver, thyroid, etc)

an adaptive response to increased workload or to increased neurohormonal stimuli

Question 20

the most consistent features of irreversible injury

Answer 20

profound membrane damage

inability to restore mitochondrial function

severe DNA or protein damage

Question 21

necrosis vs apoptosis

Answer 21

necrosis is cell death that WILL incite an inflammatory reaction. Cytoplasmic contents WILL leak out

apoptosis is cell death that WILL NOT incite an inflammatory reaction. Cytoplasmic contents WILL NOT leak out

Question 22

necrosis overview

Answer 22

‘accidental’ death because of something such as ischemia or hypoxia or toxic insult of some type

cell contents are released outside of the cell and an inflammatory response will be elicited

Question 23

apoptosis overview

Answer 23

cell death triggered by extracellular or intracellular stimuli and performed thru organized cellular signaling pathways (cascades)

an inflammatory response is not elicited

Question 24

coagulative necrosis

Answer 24

a type of necrosis that preserves the tissue architecture for a span of at least a few days

it is the pattern associated with hypoxia in all organs except the brain

localized areas of coagulative necrosis called infarcts; further characterized as pale or red depending on the presence of collateral vasculature

Question 25

liquefactive necrosis overview

Answer 25

transformation of dead tissue into a liquid viscous mass

it is the pattern associated with hypoxia in the brain and in bacterial abscesses

Question 26

caseous necrosis

Answer 26

cheeselike-appearance; most often associated with tuberculosis

Question 27

fat necrosis

Answer 27

released fatty acids combined with calcium to produce chalky-white deposits (fat saponification)

commonly associated with pancreatitis (as the enzymes spill out and release pancreatic enzymes (phospholipids, proteases, lipase) into the surrounding tissues)

Question 28

gangrenous necrosis

Answer 28

the clinical term usually applied to coagulative necrosis of a limb

called wet gangrene when there is superimposed bacterial infection with liquefactive necrosis

Question 29

infarcts

Answer 29

localized areas of coagulative necrosis

Question 30

necrosis at the cellular level

Answer 30

cell and organelle swelling

ATP depletion

increased plasma membrane permeability

the release of macromolecules from the cell

eventually, cell death

Question 31

response to necrosis

Answer 31

usually acute inflammation

Question 32

types of necrosis

Answer 32

coagulative necrosis

liquefactive necrosis

fat necrosis

caseous necrosis

fibrinoid necrosis

Question 33

liquefactive necrosis mechanism

Answer 33

occurs when the rate of dissolution of necrotic cells is faster than the rate of repair

PMN’s respond and their hydrolases digest dead cells, causing an abscess

Question 34

fibrinoid necrosis

Answer 34

an alteration of injured blood vessels where plasma proteins accumulate beneath the intima

signifies vessel damage has occurred and frequently, a marker for systemic vasculitis

Question 35

pyknosis

Answer 35

a change that occurs in cell death in which the nucleus shows an irreversible condensation of chromatin

Question 36

karyorrhexis

Answer 36

a change that occurs in cellular death in which the nucleus fragments and its chromatin is distributed irregularly.

Question 37

karyolysis

Answer 37

a late nuclear change that occurs in cell death in which the nucleus dissolves or appears faint due to decreased affinity for basic stains

Question 38

cytoplasmic changes in cell death

Answer 38

increased eosinophilia (become redder)

increased cytoplasmic homogenous appearance (glassy)

vacuolated cytoplasm (multiple small holes form)

myelin figures become numerous

calcium soap formation