Pathology: Non-Plastic Disorder

Front 1

Define Adaptation

Back 1

Adaptations are reversible changes in the number, size,phenotype, metabolic activity, or functions of cells in response to changes in their environment.

Front 2

Write out the ADAPTATION MECHANISMS

Back 2

ADAPTATION MECHANISMS • Hyperplasia • Hypertrophy • Metaplasia • Atrophy

Front 3

An increase in the number of cells in an organ or tissue thus an increase in size. Is called

Back 3

Hyperplasia

Front 4

Only labile or stable cells capable of cell division become hyperplastic. T/f

Back 4

Non-dividing cells do not (e.g. myocardium and skeletal muscle)

Front 5

Cell proliferation ceases when stimulus stops unlike in neoplasia. T/f

Back 5

True

Front 6

Cell proliferation is initiated by _________

Back 6

Growth factors, hormones andcytokines

• Cytokines: TNF, IL-6

• Growth factors

• Transforming growth factor (TGF)

• Epidermal growth factor

• Hepatocyte growth factor

• Platelet-derived growth factor

Front 7

Mention two examples of physiological Hyperplasia

Back 7

• Hormonal, eg

-Breast at puberty,

-Pregnancy and lactation; uterus in pregnancy

• Compensatory, eg

following partial hepatectomy.

TFG-ά andhepatocyte growth factor stimulate the cell proliferation

Front 8

Give two examples of pathological Hyperplasia

Back 8

• Excess hormone:

-Endometrial hyperlasia due to oestrogen/progestorone imbalance.

-BPH due to androgen.

• Chronic irritation/ Injury: Connective tissue response in keloidform

Front 9

Increase in the size of the tissue or organ due to increase in the size of cells. Is termed what

Back 9

Hypertrophy

Front 10

Pathological hyperplasia can act as a fertile soil for cancer

Back 10

True

Front 11

Hypertrophy Occurs in tissues incapable of cell division. T/f

Back 11

True

Occurs in non-dividing cells such as cardiac, skeletal and smooth muscle as a response to increased workload.

Front 12

Hypertrophy is induced by:

Back 12

Growth factors:• Transforming growth factor-β (tgf-β)• Insulin-like growth factor (IGF)• Fibroblast growth factor (FGF)

Hypertrophy agonists:• a-adrenergic agonists• Endothelin-i• Angiotensin-ii• Nitric oxide (NO)• Bradykinin

Front 13

Mention 3 causes of hypertrophy

Back 13

Hypertrophy:

• 1. Increased synthesis of contractile proteins

• 2. Induction of embryonic/fetal genes

• 3. Increased production of growth factors

Front 14

List the physiological causes of hypertrophy

Back 14

Physiologic

• Uterus during pregnancy (hypertrophy & hyperplasia)

• Skeletal muscle hypertrophy e.g. athletes and manual labourers

Front 15

Hypertrophy could be

Back 15

• Functional- Exercise

• Compensatory- kidney

• Obstructive- GIT

• Hormone mediated- Anabolic steroids

Front 16

List the pathological causes of Hypertrophy

Back 16

Pathologic:

• Myocardial hypertrophy in hypertension

• Smooth muscle hypertrophy e.g.

- Cardiac achalasia (in oesophagus)• Pyloric stenosis (in stomach)

Front 17

Shrinkage in the size of cell by loss of cell substance is called ______

Back 17

Atrophy

Front 18

List major causes of atrophy

Back 18

Atrophy is due to:

• Decreased workload

• Loss of innervation

• Diminished blood supply

• Inadequate nutrition

• Loss of endocrine stimulation

• Aging- senile atrophy

Front 19

Cellular atrophy results from a combination of decreased protein synthesis and increased protein degradation. T/f

Back 19

True

Front 20

In many situations, atrophy also is associated with autophagy, with resulting increases in the number of autophagic vacuoles. T/f

Back 20

True

Front 21

List the examples of Physiological atrophy:

Back 21

• During fetal development: e.g. atrophy of embryonic structures such as thyroglossal duct.

• During adult life: e.g. involution of thymus, atrophy of brainand heart due to aging (senile atrophy).

Front 22

List the examples of pathological atrophy

Back 22

1. Local - Disuse atrophy (decreased workload): Immobilization/ prolonged bed rest. - Denervation atrophy: Poliomyelitis - Ischemic atrophy: Brain atrophy produced by ischemia due to atherosclerosis of the carotid artery. - Pressure atrophy: Renal parenchyma atrophy in hydronephrosis due to increased pressure. 2. Generalized - Starvation atrophy: Protein-calorie malnutrition

Front 23

A reversible change in which one adult cell type (eg epithelial) is replaced by another adult cell type is termed

Back 23

Metaplasia

Front 24

Metaplasia in certain cases may progress to ______&_______

Back 24

Dysplasia and Neoplasia

Front 25

Substitution of more sensitive cells by cell types better able to withstand stress and adverse conditions is also termed metaplasia. T/f

Back 25

True

Front 26

_______ mechanism is Due to re-programming of stem cells or undifferentiated mesenchymal cells to adifferent cell type • Both extra- and intra-cellular signals induce transcription of genes controlling differentiation along new pathway.

Back 26

Metaplasia

Front 27

Mention two examples of metaplasia

Back 27

1. Epithelial Metaplasia

• Squamous metaplasia:

• Respiratory tract: e.g. chronic irritation due to tobaccosmoke

• Cervix: associated with chronic infection.

• Columnar metaplasia:

• Squamous to columnar: Barrett esophagus

• Intestinal metaplasia

2. Connective Tissue Metaplasia

• Osseous metaplasia: New bone at sites of tissue injury.Myositis ossificans- usually following intramuscular hemorrhage.

Front 28

DYSPLASIA

• Deranged development

• Proliferation with associated cytological atypia (size, shapeand organization)

• Not an adaptive process

• Sometimes called atypical hyperplasia• Usually accompanies adaptive changes• A precursor of neoplasia.

T/f

Back 28

True

Front 29

HYPOPLASIA • Reduction in size of cells and tissue • Mech: Failure of growth to normal size

T/f

Back 29

True

Front 30

APLASIA• Also called ________

Back 30

Agenesis

• The complete failure of growth of an organ or part atembryogenesis• Seen in genetic disorders e.g amelia