Cellular Adaptations Al-Quds University - PowerPoint Presentation

Slide1

Cellular Adaptations

Al-Quds University

Assistant professor of pathology.Faculty of MedicinePathology Department

1

Slide2

2

Cellular

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

Slide3

3

1)

Physiological adaptationresponses of cells to normal stimulation by hormones or endogenous chemical mediatorse.g. hormones leading to enlargement of the breast and the uterus during pregnancy

2)

Pathological adaptation

allows the cells to modulate their environment and ideally escape injury

e.g.

hormones produced by tumors leading to endometrial hyperplasia

Cellular Adaptation

Slide4

4

up- or down-regulation

of specific cellular receptorsreceptor bindingIncrease or decrease of protein synthesisswitch from producing one type of protein to another

Mechanisms of Cellular Adaptation

Slide5

5

Cellular adaptation

Types of adaptive responses:Atrophy - decrease in cell sizeHypertrophy - increase in cell sizeHyperplasia

- increase in cell numberMetaplasia - change in cell type 

Others:

aplasia

,

hypoplasia

Slide6

6

necrosis

reversible

irreversible

cell injury

adaptation

hypertrophy

hyperplasia

metaplasia

dysplasia

normal bronchial epithelial cell

atrophy

Cellular Adaptation to stress

Slide7

7

Atrophy

Shrinkage in the size of the cell by loss of cell substances, 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

Slide8

8

Causes of Atrophy

1) Physiological:thymic involution, agingloss 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

Slide9

9

A

, Atrophy of the brain in an 82-year-old male with atherosclerotic disease. Atrophy of the brain is due to aging and reduced blood supply. The meninges have been stripped. B, Normal brain of a 25-yr-old male. Note that loss of brain substance narrows the gyri and widens the sulci

Slide10

10

These kidneys are from a patient who had atherosclerotic stenosis of one renal artery

Normal

Slide11

11

Mechanisms of Atrophy

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

apoptosis

Slide12

12

Atrophy:

increase catabolismProteolytic systems for degradation:1) Lysosomes contain hydrolases and other enzymesdegrade exogenous proteins

engulfed by endocytosis degrade subcellular components (e.g. organelles) leading to the formation of autophagic vacuoles

Slide13

13

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

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.

Ubiquitin:

Slide14

14

The ubiquitin-proteasome pathway:

Slide15

Hypertrophy

Increase in the size of cells 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

15

Slide16

Causes of Hypertrophy:

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

16

Slide17

Mechanisms of Hypertrophy

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

17

Slide18

hypertrophy after myocardial infarction

The mechanisms of cardiac hypertrophy:

mechanical triggers, such as stretchtrophic triggers, such as activation of α-adrenergic receptors

18

Slide19

Hypertrophy in hypertension

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

Reactivation of certain genes. Switch of contractile proteins to a different type. Degenerative changes overtime leading to failure of organ19

Slide20

Skeletal muscle hypertrophy in body building:

20

Slide21

Hyperplasia

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 DIVIDE21

Slide22

22

Gravid uterus

Hyperplasia

Slide23

Causes of Hyperplasia:

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)

23

Slide24

Hyperplasia

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

This differentiates these processes from cancer, in which cells continue to grow despite the absence of hormonal stimuli. pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation may eventually arise. e.g. patients with hyperplasia of the endometrium are at increased risk of developing endometrial cancere.g. papillomavirus infections predispose to cervical cancers

24

Slide25

Hypertrophy & hyperplasia

Summary

25

Slide26

Metaplasia

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.the influences that induce metaplastic transformation, if persistent, may induce cancer transformation in the metaplastic epithelium

26

Slide27

Examples of Metaplasia

(respiratory epithelium)

27

Slide28

Metaplastic transformation of esophageal stratified squamous epithelium

(left)

to mature columnarepithelium (so-called Barrett metaplasia)

28