Cellular Adaptions

Question 1

A new steady state which lies between normal unstressed cell, and the injured overstressed cell, in which the cell can function and preserve viability.

Answer 1

Cellular Adaptation

Question 2

responses of cells to normal stimulation by hormones or endogenous chemical mediators
e.g. hormones leading to enlargement of the breast and the uterus during pregnancy

Answer 2

) Physiological adaptation

Question 3

allows the cells to modulate their environment and ideally escape injury
e.g. hormones produced by tumors leading to endometrial hyperplasia

Answer 3

Pathological adaptation

Question 4

Mechanisms of Cellular Adaptation

Answer 4

up- or down-regulation of specific cellular receptors
receptor binding
Increase or decrease of protein synthesis
switch from producing one type of protein to another

Question 5

change in cell type
Replacement of one type of adult cell, whether epithelial or mesenchymal, by another type of adult cell
aiming at replacing cells that are sensitive to certain stimuli by a more resistant cell type.
This happens through reprogramming of stem cells or undifferentiated mesenchymal cells.

Answer 5

Metaplasia

Question 6

an increase in the size of the organ due to increase in the number of the cells in the organ, leading to increase in the function.
SEEN IN CELLS THAT CAN DIVIDE

Answer 6

Hyperplasia

Question 7

Increase in cell size by an increase in the number and density of the cellular substances, leading to an over all increase in the size and the function of the organ, and a new equilibrium is reached.
Mainly occurs in organs composed of cells that can’t divide (cardiac & skeletal muscles).
NO NEW CELLS, JUST BIGGER CELLS

Answer 7

Hypertrophy

Question 8

Decrease in cell size
, leading to diminished function of the cell and a new equilibrium is reached.
Accompanied by decrease in the organ size, if sufficient number of cells is involved.
The cells are not dead

Answer 8

Atrophy

Question 9

Causes of atrophy

Answer 9

Physiological:
thymic involution, aging
loss of hormonal stimuli (menopause)
2) Pathological:
decrease work load (immobilization of a limb to permit healing of a fracture)
loss of innervation (Denervation atrophy)
diminished blood supply (ischemic atrophy)
inadequate nutrition

Question 10

Mechanism of atrophy

Answer 10

Imbalance between protein synthesis and degradation is the fundamental step, leading to reduction in structural components.
Decreased synthesis, increased catabolism, or both
the fundamental cellular changes are identical in physiological and pathological causes.
Sometimes the number of cells can be reduced by the process apoptosis

Question 11

Proteolytic systems for degradation

Answer 11

1) Lysosomes contain hydrolases and other enzymes
degrade exogenous proteins engulfed by endocytosis
degrade subcellular components (e.g. organelles) leading to the formation of autophagic vacuoles
2) The ubiquitin-proteasome pathway:

Degradation of cytosolic and nuclear proteins
Responsible for the accelerated proteolysis in hypercatabolic
states (e.g. cancer)
The protein/ubiquitin complexes are engulfed by the cytoplasmic
proteasome

Question 12

An abundant protein found in normal cells.
It has a role in removing old or damaged proteins by acting as a cofactor for proteolysis.
** Proteasomes: non lysosomal proteinases

Answer 12

Ubiquitin

Question 13

Causes of hypertrophy

Answer 13

Physiological or pathological:
Increase in functional demand or work load e.g. body building, hypertension, aortic valve disease

Increase in hormonal stimulation. This involves both hypertrophy and hyperplasia and both result in an enlarged (hypertrophic) organ.

Question 14

Gravid uterus type of adaptation?

Answer 14

the gravid uterus occurs as a consequence of estrogen stimulation of both smooth muscle hypertrophy and smooth muscle hyperplasia

Question 15

Mechanism of Hypertrophy

Answer 15

an increased synthesis of structural proteins and organelles leading to an overall increase in the workload of the organ.

Question 16

The mechanisms of cardiac hypertrophy

Answer 16

mechanical triggers, such as stretch

trophic triggers, such as activation of α-adrenergic receptors

Question 17

Adaptive changes may not be completely benign; they can also result in a dramatic change in the cellular phenotype:

Answer 17

Reactivation of certain genes.
Switch of contractile proteins to a different type.
Degenerative changes overtime leading to failure of organ

Question 18

Causes of Hyperplasia

Answer 18

Physiological:
hormonal hyperplasia (e.g. female breast at puberty and during pregnancy)
compensatory hyperplasia: occurs when a portion of the tissue is removed or diseased which is under the influence of growth factors (e.g. liver resection, wound healing)
Pathological:
Under the effect of hormones or growth factors. (e.g. Endometrial hyperplasia, skin wart)

Question 19

Both hypertrophy and hyperplasia are ………., if the stimulus is removed

Answer 19

Reversible

Question 20

pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation may eventually arise.

Answer 20

. patients with hyperplasia of the endometrium are at increased risk of developing endometrial cancer
e.g. papillomavirus infections predispose to cervical cancers

Question 21

Vitamin A deficiency causes

Answer 21

Metaplasia

Question 22

Atp functions

Answer 22

the maintenance of cellular osmolarity
transport processes
protein and lipid synthesis
basic metabolic pathways

Question 23

: unstable chemical species with a single unpaired electron in the outer orbital

Answer 23

Free radicals

Question 24

Free radicals

Answer 24

1) Reactive nitrite species
2) Oxygen free radicals or reactive oxygen species (ROS) include:
Superoxide anion radicals (O2-)
Hydrogen peroxide (H2O2)
Reactive hydroxyl radical (HO.)

Question 25

Sources of Free radicals

Answer 25

Inflammation
Radiation
Oxygen toxicity
Chemicals
Reperfusion injury

Question 26

Targets of free radicals

Answer 26

DNA fragmentation

Protein cross-linking and fragmentation

Question 27

may either block the formation of free radicals or scavenge them

Answer 27

Endogenous or exogenous antioxidants (e.g., vitamins E, A, and C, and β-carotene)

Question 28

), Hg binds to the sulfhydryl groups of cell membrane proteins, causing inhibition of ATPase-dependent transport and increased membrane permeability.

Answer 28

Mercuric chloride poisoning (HgCl2)

Question 29

Carbon tetrachloride (CCl4)

Answer 29

Used in dry cleaning

Converted to the toxic free radical CCl3· in the liver