Summer Patho

Question 1

Etiology

Answer 1

is the origin of disease, underlying causes and modifying factors. -WHY a disease develops)

Question 2

Pathogenesis

Answer 2

refers to the steps of in the development of the disease -( HOW a disease develops)

Question 3

Morphology

Answer 3

Changes in gross or microscopic appearance of cells and tissues and biochemical alterations in body fluids (blood and urine).

Question 4

Adaptation

Answer 4

achieving a new steady state and preserving viability and function.

Question 5

Principal adaptive responses are;

Answer 5

hypertrophy, hyperplasia, atrophy, metaplasia

Question 6

Causes of cell death:

Answer 6

Ischemia, infections, toxins, and immune reactions.

Question 7

CELL DEATH

Answer 7

is a normal and essential process in embryogenesis, the development of organs, and the maintenance of homeostasis.

Question 8

Hypertrophy

Answer 8

(an increase in the size of the individual cells & ultimately the entire heart)- Myocardium subjected to persistent increased load, as in hypertension or with a narrowed stenotic valve adapts by undergoing hypertrophy.

Question 9

3 processes that affect cells and tissues:

Answer 9

intracellular accumulations, pathological calcification, and cell aging.

Question 10

Adaptations

Answer 10

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

Question 11

Physiologic adaptation

Answer 11

represent responses of cells to normal stimulation by hormones or endogenous chemical mediators (ex.- the hormone-induced enlargement of the breast and uterus during pregnancy).

Question 12

Pathologic adaptations

Answer 12

responses to stress that allow cells to modulate their structure and function and thus escape injury.

Question 13

Hypertrophy

Answer 13

increase in the size of cells resulting in an increase size of the organ. NO NEW CELLS JUST BIGGER CELLS. -can be physiologic or pathologic.

Question 14

Hyperplasia

Answer 14

an adaptive response in cells capable of replication. Increase # of cells - increased organ size.

Question 15

Mechanisms driving cardiac hypertrophy;

Answer 15

mechanical triggers-stretch

trophic triggers- soluble mediators that stimulate cell growth, such as adrenergic hormones.

Question 16

Hyperplasia

Answer 16

Can be physiologic (1.hormonal hyperplasia-proliferation of the glandular epithelium of the female breast 2. Compensatory hyperplasia- residual tissue grows after removal or loss of part of an organ)
and pathologic.

Question 17

Pathologic hyperplasia

Answer 17

caused by excessive hormonal or growth factor stimulation.

Question 18

Atrophy

Answer 18

Shrinkage in the size of the cell by the loss of cell substance. Cells decrease in size, therefore organ size diminishes. Diminished function but are not dead. Decreased workload, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging.

Question 19

Mechanisms of atrophy

Answer 19

consist of a combination of decreased protein synthesis and increased protein degradation in cells.

Question 20

Metaplasia

Answer 20

a reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult type.

Question 21

Reversible cell injury

Answer 21

If the damaging stimulus is removed, the injury has typically not progressed to severe membrane damage and nuclear dissolution.

Question 22

Cell death

Answer 22

Continuing damage, the injury becomes irreversible, the cell cannot recover and it dies.

Question 23

2 types of cell death

Answer 23

1. Necrosis- damage to membranes is severe, enzymes leak out lysosomes, enter the cytoplasm, and digest the cell.
2. Apoptosis - When a cell is deprived of growth factors or the cell’s DNA or protein are damaged beyond repair, the cell kills itself.

Question 24

Causes of cell injury:

Answer 24

Oxygen deprivation, chemical agents, infectious agents, immunologic reactions, genetic factors, nutritional imbalances, physical agents, aging.

Question 25

Fibrinoid necrosis

Answer 25

Only detected by histological examination

Question 26

Coagulative necrosis

Answer 26

Affected tissues become firm, the injury denatures structural proteins and enzymes. It is also a characteristic of INFARCTS (areas of ischemia necrosis) in all of the solid organs except the brain.

Question 27

Liquefactive necrosis

Answer 27

seen in focal bacteria, fungal infections, because microbes stimulate the accumulation of inflammatory cells and enzymes of leukocytes digest (liquefy) the tissue. Tissue liquefied due to hydrolytic enzymes from tissue and/or PMNs
See in abscesses and CNS tissue

Question 28

Gangrenous necrosis

Answer 28

Condition of the limb, that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers.

Question 29

Caseous (“cheese-like”) necrosis

Answer 29

often in foci of tuberculous infection. Yellow white appearance of the area of necrosis.ype of necrosis which is a collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border.

Question 30

Fat necrosis

Answer 30

refers to focal areas of fat destruction, resulting from the release of activated pancreatic lipase’s into the substance of the pancreas and the peritoneal cavity.

Question 31

types of fat necrosis (3)

Answer 31

Enzymatic necrosis (pancreatic necrosis of fat)Traumatic necrosisNecrosis of abdominal fat of cattle.

Question 32

Fibrinoid necrosis

Answer 32

Bright pink and amorphous ‘hyaline’ deposits of immune complexes (Ags + Abs), complements with leaked out fibrin in the walls of arteries; not a true type of necrosis