Cellular Responses to Stress and Toxic Insults: Adaptations, Injury, and Death

Question 1

Hypertrophy

Answer 1

Increase in size of cell via growth factors

Question 2

Physiologic Hypertrophy

Answer 2

Seen during increased demand such as exercise (skeletal muscle hypertrophy)

Question 3

Pathologic Hypertrophy

Answer 3

Hypertrophic heart due to hypertension

Via gene protein synthesis and production of orgenelles

Question 4

Selective hypertrophy

Answer 4

Increase in size of subcellular organelle
Example: barbiturates (hypertrophy of the SER)
Alcohol intake (hypertropgy of the SER)

Question 5

Hyperplasia

Answer 5

Increase in the number of cells that also cause increase in organ mass from stem cells

Question 6

Physiologic Hyperplasia

Answer 6

Hormone induced: growth of breasts in puberty, gravid uterus

Compensatory Hyperplasia: regeneration of liver after partial hepatectomy

Question 7

Pathologic Hyperplasia

Answer 7

Occurs due to underlying pathologic process, incred risk for cancer; driven by growth factors/hormones

Endometrial Hyperplasia from PCOD –> Malignant transformation (endometrial carcinoma)

Prostatic Hyperplasia –> BPH, no malignancy

Viral infections: HSV, no malignancy

Question 8

Atrophy

Answer 8

Apoptosis (Decrease in cell number)

Autophagy - ubiquitin decrease in cell size

Question 9

Physiologic Atrophy

Answer 9

Notochord and thyroglossal duct undergo atrophy during feta development,
If duct persists –> thyroglossal dust

Question 10

Pathologic Atrophy

Answer 10

1 - Decreased work load (disuse atrophy)
2 - Loss of innervation (nerve damage)
3 - Diminished blood supply (may eventually lead to apoptosis of cells/organs –> renal and spleen arteries
4 - Sickle cell repeated vasculoocclusive cyst
5 - Inadequate nutrition
6 - Loss of endo stimulation
7 - Pressure induced atrophy (tumor)

Via ubiquitin-proteasome pathway: cytoskeleton breaksdown; overactivity –> cancer cachexia

Question 11

Atrophic cells residual bodies

Answer 11

Residual bodies are the parts not digested during autophagic lysosomal digestion

Question 12

Atrophic residual bodies example: Brown atrophy of the heart/liver in elderly from lipofuscin granules

Answer 12

From lipofuscin granules found in cytoplasm

Question 13

Metaplasia

Answer 13

Reversible change in which one differentiated cell type is replaced by another type of cell.

Occurs in epithelial and connective tissues

Question 14

Metaplasia Epithelial Examples (2)

Answer 14

At risk for malignancy

1. Smoker: ciliated columnar is replaced by squamous epithelium (at risk for squamous cell carcinoma)
2. Barret esopohagus: lower esophagus squamous epithelium is replaced by intestinal epithelium with goblet cells (intestinal metaplasia) –> at rish for adenocarcinoma of the esophagus

Question 15

Connective Tissue Metaplasia (no malignancy)

Answer 15

Myositis Ossificans: formation of bone in connective tissue

No malignancy

Question 16

Other sites of metaplasia

Answer 16

Vit. A deficiency/keratomalacia: sqaumous metaplasia of the respiratory tract and urinary tract, thickness of conjunctivia

Question 17

Metaplasia mechanism:

Answer 17

Reprogramming of stem cells and it’s signaling.

E.g. Tx of GERD: decrease in acid

Question 18

Causes of cell injury (7)

Answer 18

1. oxygen deprivation
2. Physical agents
3. Chemical agents and drugs
4. Infectious agents
5. Immunologic rxns
6. Genetic derangments
7. Nutritional imbalances

Question 19

Necrosis:

Answer 19

Leaks contents
Associated with inflammaation
Pyknosis–> karyorrhexis –> karyolysisi
Pathologic

Question 20

Apoptosis

Answer 20

No leakage of contents
No inflammation
Reduced shrinkage
Nucleosome fragmentation 
Pathologic 
Physiologic (often)

Question 21

Morphologic Changes in Cell Injury

Answer 21

Cellular swelling (ion pumps fail in membrane)
Small clear vacuoles in cytoplasm
Incresed in eosinophilic staining

Question 22

Ultra structural changes of cell injury: plasma membrane

Answer 22

Blebbing (early ischemia), blunting, loss of microvilli

Question 23

Ultra structural changes of cell injury : mitochondria

Answer 23

swelling and amorphous densities

Question 24

Ultra structural changes of cell injury : ER

Answer 24

Dilatation, detachment of polysomes, intracytoplasmic myelin figures

Question 25

Ultra structural changes of cell injury: Nucleus

Answer 25

disaggregation of granular and fibrallar elements

Question 26

Necrosis:

Answer 26

result of denaturation of intracellular proteins and enzymatic digestion of lethally injured cells

Question 27

Necrosis: morphologic changes

Answer 27

Increased eosinophilia, glassy homogenous experience

Question 28

Necrosis: nuclear changes

Answer 28

Pyknosis: nuclear shrinking, increased basaphilia,
Karyarrhexis: fragmentation of pyknotic nucleus
Karyolysis: fading of the basophilia of the chromatin

Question 29

Types of Necrosis (6)

Answer 29

Coagulative, Liquefactive, Gangrenous, Caseous, Fat, Fibrinoid

Question 30

Coagulative

Answer 30

Preservation of the structural outline of dead cells; nucleus disappears
WEDGE-SHAPED
Spleen, Kidney, and heart