Chapter 2

Question 1

hypertrophy

Answer 1

increased cell and organ size due to increased work load
stimulus - mechanical stress, agonists, GF leads to activation of signal transduction pathways
effects - induction of embryonic/fetal genes, increased synthesis of proteins, increased production of GF
occurs in - cardiac mm, skeletal mm, and nerves

Question 2

hyperplasia

Answer 2

increased cell numbers in response to hormones and GF
mechanism - increased cell production from stem cells
physiologic - due to action of hormones, need to increase functional capacity of organs or compensatory increase after damage
pathologic - excessive or inappropriate actions of hormones of GF acting on target cells

Question 3

atrophy

Answer 3

decrease in cell and organ size due to decreased nutrient supply or disuse
can be physiologic or pathologic
decreased cell number - apoptosis
decreased cell size - ubiquitin proteasomal pathway and increased autophagy

Question 4

metaplasia

Answer 4

change in phenotype of epithelial or mesenchymal cells due to response to chronic irritation that makes cells better to withstand stress
mechanism - reprogramming of stem cells that are known to exist in normal tissues or undifferentiated mesenchymal cells present in CT

Question 5

reversible cell injury

Answer 5

cellular swelling due to changes in ion concentrations and water influx
reduced oxidative phosphorylation w/ resultant depletion of ATP

Question 6

irreversible cell injury

Answer 6

membrane damage

necrosis or apoptosis

Question 7

necrosis

Answer 7

cell size - enlarged (swelling)
nucleus - pyknosis, karyorrhexis, karyolysis
plasma membrane - disrupted
cellular contents - enzymatic digestion, may leak out of cell
adjacent inflammation - frequent
physiologic or pathologic role - invariably pathologic

Question 8

apoptosis

Answer 8

cell size - reduced (shrinkage)
nucleus - fragmentation into nucleosome-size fragments
plasma membrane - intact, altered structure, orientation of lipids
cellular contents - intact, may be released in apoptotic bodies
adjacent inflammation - no
physiologic or pathologic role- often physiologic, may be pathologic

Question 9

karyolysis

Answer 9

basophilia of chromatin fade

due to loss of DNA by enzymatic degradation by endonucleases

Question 10

pyknosis

Answer 10

nuclear shrinkage and increased basophilia

chromatin condense

Question 11

karyorrhexis

Answer 11

fragmentation of pyknosis nucleus

Question 12

coagulative necrosis

Answer 12

architecture of dead tissue is preserved
tissue has firm texture
nucleus not present
presence of phagocytosis and leukocytes through lysosomes
caused by ischemia causes by obstruction in vessel (infarct)
not seen in the brain

Question 13

liquefactive necrosis

Answer 13

digestion of the dead cells leading to the tissues becoming a liquid viscous mass
seen in bacterial or fungal infections
creamy yellow due to leukocytes
caused by hypoxic death of cells w/in CNS
seen in brain, abscess, and pancreatitis

Question 14

gangrenous necrosis

Answer 14

seen in limb that has undergone coagulative necrosis
liquefactive necrosis is also seen - wet gangrene
seen in lower limb and GI tract

Question 15

caseous necrosis

Answer 15

friable and white cheese like
seen w/ tuberculous (fungal infection)
structure less collection of fragmented or lysed cells and amorphous granular debris enclosed w/in distinctive inflammatory border

Question 16

fat necrosis

Answer 16

focal areas of fat destruction due to pancreatic lipase activity or trauma
chalky white appearance due to deposition of Ca
shadowy outlines of necrotic fat cells w/ basophilic Ca deposits surrounded by an inflammatory reaction

Question 17

fibrinoid necrosis

Answer 17

abs and ags complexes are deposited in the walls of a along with fibrin
bright pink and amorphous
seen in blood vessels due to malignant hypertension or vasculitis

Question 18

depletion of ATP

Answer 18

decrease in Na dependent pump - ion imbalance and cellular swelling
increase in anaerobic glycolysis - decrease in pH leads to clumping of nuclear chromatin
detachment of ribosomes - decrease protein synthesis

Question 19

superoxide

Answer 19

due to incomplete reduction of oxygen

inactivated by SOD converting to H2O2 and O2

Question 20

hydrogen peroxide

Answer 20

created by SOD and oxidases in peroxisomes

inactivated by catalase or glutathione peroxidase converting to H20 and O2

Question 21

hydroxyl radical

Answer 21

created by hydrolysis of H20

inactivated by glutathione peroxidase converting to H20

Question 22

ONOO

Answer 22

creased by superoxide and NO through NO synthase

inactivated by peroxiredoxins to HNO2

Question 23

cystic fibrosis

Answer 23

affected protein - CFTR

pathogenesis - defects in Cl transport

Question 24

familial hypercholesterolemia

Answer 24

affected protein - LDL R

pathogenesis - hypercholesterolemia

Question 25

tay-sachs disease

Answer 25

affected protein - hexosaminidase beta subunit

pathogenesis - storage of GM2 gangliosides in neurons

Question 26

alpha-1-antitrypsin deficiency

Answer 26

affected protein - alpha 1 antitrypsin

pathogenesis - apoptosis

Question 27

creutzfeldt-jacob disease

Answer 27

affected protein - prions

pathogenesis - abnormal folidng of PrPsc leads to neuronal cell death

Question 28

alzheimer disease

Answer 28

affected protein - A beta peptide

pathogenesis - aggregation w/in neurons and apoptosis