Robbins Chapter 2 Key Concepts

Question 1

Appearance Hypertrophy

Answer 1

increase in size of the cells and organ size

Question 2

Cause of hypertrophy

Answer 2

increased workload induced by growth factors in response to mechanical stres

Question 3

What type of cells does hypertrophy occur

Answer 3

cells that are incapable of cell division

Question 4

Appearance of Hyperplasia

Answer 4

increase in cell number

Question 5

Cause of hypertrophy

Answer 5

hormones and growth factors

Question 6

What types of cells does hyperplasia occur

Answer 6

cells that are able to divide or have abundant stem cell

Question 7

Appearance of atrophy

Answer 7

decreased size of the cell or organ

Question 8

Cause of atrophy

Answer 8

decreased nutrient supply or disuse
increased breakdown of cellular organelles
decreases synthesis of cellular building blocks

Question 9

Appearance of metaplasia

Answer 9

change in phenotype of differentiated cells

Question 10

Cause of metaplasia

Answer 10

chronic irritation that causes change in cell type to better accommodate the changed phenotype

Question 11

Results of metaplasia

Answer 11

reduced function and increased risk for malignancy

Question 12

Reversible cell injury characteristics

Answer 12

cellular swelling
fatty change
plasma membrane blebbing 
mitochondrial swelling 
dilation of ER,
eosinophilia

Question 13

Necrosis characteristics

Answer 13

increased eosinophilia 
nuclear shrinkage
fragmentation
dissolution
breakdown of plasma membrane 
myelin figures
leakage and enzymatic digestion of cell contents

Question 14

Patterns of tissue necrosis (6)

Answer 14

coagulative, liquefactive, caseous, gangrenous, fat, fibrinoid

Question 15

Mechanisms of cell injury (6)

Answer 15

ATP depletion
Mitochondrial damage
Influx of Ca+
Accumulation of ROS
Increased permeability of membrane
Accumulation of damaged DNA and misfolded proteins

Question 16

Cell injury by ATP depletion

Answer 16

failure of energy dependent functions –> reversible injury –> necrosis

Question 17

Cell injury by Mitochondrial damage

Answer 17

ATP depletion –> failure of energy dependent functions –> necrosis or potentially apoptosis

Question 18

Cell injury by influx of calcium

Answer 18

activation of enzymes that damage cellular components

can trigger apoptosis

Question 19

Cell injury by Accumulation of ROS

Answer 19

covalent modification to lipids, proteins, and nucleic acids

Question 20

Cell injury by increased permeability of membrane

Answer 20

affects plasma membranes, lysosomal membranes, mitochondrial membranes
results in necrosis

Question 21

Mild Ischemia

Answer 21

reduced oxidative phosphorylation –> reduced ATP –> failure of Na pump –> influx of sodium and water –> cause cell swelling

Question 22

Severe/prolonged Ischemia

Answer 22

severe swelling of mitochondria –> calcium influx –> rupture of lysosomes and plasma membrane –> death due to necrosis and apoptosis via release of cytochrome c

Question 23

Reperfusion Injury

Answer 23

oxidative stress –> blood flows to ischemic area –> influx of calcium –> influx of leukocytes –> local activation of classical complement system

Question 24

Apoptosis definition

Answer 24

regulated cell death that eliminates unwanted or irreparable damaged cells with least host reaction

Question 25

Characteristics of apoptosis

Answer 25

enzymatic degradation of proteins and DNA
DNA damage
accumulation of misfolded proteins
pro-apoptotic proteins activated
anti-apoptotic proteins inhibited

Question 26

Death Receptor (Extrinsic) Pathway function

Answer 26

elimination of self-reactive lymphocytes and damage by CTLs

Question 27

How is the Death Receptor (extrinsic) pathway initated

Answer 27

death receptor (TNF receptor family) engagement by ligands