Ch 4. Altered Cellular and Tissue Biology

Question 1

When does a cell become irreversibly injured?

Answer 1

Once changes to the nucleus occur and cell membranes are disrupted, the cell moves to irreversible injury and death.

Question 2

Pathology

Answer 2

Conditions typically observed during a disease state.

Question 3

Physiology

Answer 3

Biological discipline that describes processes or mechanisms operating within an organism

Question 4

Discuss the pathogenesis of hypoxic injury?

Answer 4

Decreased ATP production, leading to Na and Ca accumulation, acute swelling, decreased protein synthesis, lipid deposition, and anaerobic glycolysis.

Question 5

What are the mechanisms of ischemia-reperfusion injury?

Answer 5

• Oxidative stress - Reoxygenation causes the increased generation of reactive oxygen species (ROS) and nitrogen species.
• Increased intracellular Ca cxn
• Inflammation- danger signals from cytokines are released by resident immune cells when cells die.
• Complement activation

Question 6

Why are children more susceptible to the toxic effects of lead exposure?

Answer 6

1. More prone to hand-to-mouth behavior. Ingestion of Pb dust.
2. blood-brain barrier is immature during fetal development, contributing to greater accumulation in developing brain.
3. infant absorption of Pb is greater than in adults and bone turnover from skeletal growth results in continuous leaching of Pb into blood, causing constant body exposure.

Question 7

Discuss the sources of lead exposure?

Answer 7

Particulate lead from smelters, and previous leaded gasoline emissions. Drinking water, particularly well water. Paint.

Question 8

Discuss the mechanisms of cell injury related to chronic alcoholism?

Answer 8

Nutritional factors - Mg, Vit B6, thiamine, phosphorous, and folic acid deficiencies.
Limits intestinal absorption of folate, leading to fetal alcohol syndrome.

Question 9

What are the sources of mercury exposure?

Answer 9

gold mines, natural emissions, coal plants.

Question 10

Anoxia

Answer 10

Total lack of oxygen.

Question 11

Vacuolation

Answer 11

Formation of vacuoles.

Question 12

Lipid Peroxidation

Answer 12

The destruction of polyunsaturated lipids (the same process by which fats become rancid), leading to membrane damage and increased permeability.

Question 13

Pathologic effects of ROS?

Answer 13

• Lipid peroxidation - membrane damage.
• Protein modifications- breakdown, misfolding.
• DNA damage - mutations.

Question 14

Pathologic effects of ROS?

Answer 14

• Lipid peroxidation - membrane damage.
• Protein modifications- breakdown, misfolding.
• DNA damage - mutations.

Question 15

Xenobiotics

Answer 15

Compounds that include toxic, mutagenic, and carcinogenic chemicals.

Question 16

Biotransformation

Answer 16

Metabolism of lipophilic xenobiotics to more hydrophilic forms by the liver.

Question 17

Toxicophores

Answer 17

Short-lived unstable highly reactive chemical intermediate products of biotrasformation. Includes electrophiles, nucleophiles, free radicals, and redox-active reactants.

Question 18

Electrophiles

Answer 18

Atom or molecule that accepts e- pair to make covalent a bond.

Question 19

Nucleophile

Answer 19

Atom or molecule that donates e- pair to electrophile to make a chemical bond.

Question 20

Protein adduct

Answer 20

Chemical bound to protein.

Question 21

e.g. Environmental factors

Answer 21

co-exposure to multiple xenobiotics.

Question 22

e.g. Pathologic factors

Answer 22

inflammation, underlying liver diseases

Question 23

e.g. Physiologic factors

Answer 23

age, gender

Question 24

e.g. Physiologic factors

Answer 24

age, gender

Question 25

Cellular Accumulation (Infiltration)

Answer 25

Intracellular accumulation of abnormal amounts of various substances and the resultant metabolic disturbances.

Question 26

e.g. Endogenous

Answer 26

a product of abnormal metabolism or synthesis

Question 27

Why is an increase in cxn of intracellular calcium injurious?

Answer 27

Can lead to dystrophic calcification. Calcium salts cluster and harden, interfering with normal cellular structure and function.

Question 28

Compare and contrast necrosis and apoptosis.

Answer 28

Necrosis - cell disintegration. Accompanied by inflammation. Cell swells. Cells die long before autolysis, cellular self-digestion.
Apoptosis - Cell shrinks. DNA clumps. Cell buds off to be phagocytized. characterized by the “dropping off” of cellular fragments called apoptotic bodies. Release chemical factors to recruit phagocytes.

Question 29

Why is apoptosis significant?

Answer 29

Cells need to die; otherwise, endless proliferation would lead to gigantic bodies.

Question 30

Define autophagy.

Answer 30

Self eating. Involves delivery of cytoplasmic contents to lysosomes for degradation. Can maintain cellular metabolism under starvation conditions and remove damaged organelles, improving survival of the cell.

Question 31

Oncosis (Vacuolar degeneration)

Answer 31

Progressive vacuolation resulting in cytoplasmic swelling.

Question 32

e.g. Endogenous

Answer 32

a product of abnormal metabolism or synthesis. Produced within the body.

Question 33

e.g. Exogenous

Answer 33

infectious agents or a mineral. Produced outside the body.

Question 34

Oncosis (Vacuolar degeneration)

Answer 34

Progressive vacuolation resulting in cytoplasmic swelling.

Question 35

Steatosis

Answer 35

Intracellular lipid accumulation.

Question 36

Diseases of lipid accumulation?

Answer 36

Tay-Sachs disease, Niemann-Pick disease, and Gaucher disease.

Question 37

Diseases of carbohydrate accumulation?

Answer 37

mucopolysaccharidoses.

Question 38

Russell bodies

Answer 38

excessive aggregates of protein.

Question 39

Cytochromes

Answer 39

Oxidative enzymes.

Question 40

Hemosiderin

Answer 40

yellow-brown pigment derived from hemoglobin. Stores excess iron in tissues. Yellowish color in bruising.

Question 41

Hemosiderosis

Answer 41

condition in which excess iron is stored as hemosiderin in the cells of many organs and tissues.

Question 42

Bilirubin

Answer 42

yellow-green pigment of bile derived from the porphyrin structure of hemoglobin.

Question 43

Jaundice (icterus)

Answer 43

Excess bilirubin within cells and tissues, causing yellowing of the skin. Occurs when level excess 1.5 to 2 mg/dl of plasma. (normal values of 0.4 to 1 mg/dl).

Question 44

4 types of necrosis

Answer 44

Coagulative, liquefactive, caseous, fatty.

Question 45

Coagulative necrosis

Answer 45

Primarily in kidneys, heart, and adrenal glands. commonly results from hypoxia. Result of protein denaturation, causes albumin to change from transparent to firm, opaque state. Area of coagulative necrosis called an infarct.

Question 46

Liquefactive Necrosis

Answer 46

Commonly results from ischemic injury to neurons and glial cells in the brain.Cells are digested by their own hydrolases, so the tissue becomes soft, liquefies, and segregates from healthy tissue, forming cysts. Can be caused by bacterial infection.

Question 47

Caseous Necrosis

Answer 47

Usually results from TB infection. combo of coagulative and liquefactive necroses. Dead cell disintegrate, but debris not completely digested by hydrolases. Tissue soft and granular.

Question 48

Fatty Necrosis

Answer 48

Lipases break down triglycerides, releasing free fatty acids that then combine with Ca, Mg, and Na ions, creating soaps (saponification). Tissue appears opaque and chalk-white.