Week 2 - Cell Adaptations, Injury and Death

Question 1

What are the cell survival requirements?

Answer 1

Constant energy supply, intact plasma membrane, efficient cellular activities, genomic integrity, controlled cell division, internal homeostatic mechanism

Question 2

When does cell injury occur?

Answer 2

When the cell is unable to adapt through hyperplasia, hypertrophy, metaplasia, etc.

Question 3

What are the types of lethal cell injury?

Answer 3

Necrosis, apoptosis

Question 4

What are the types of sub lethal cell injury?

Answer 4

Fatty change (steatosis), hydropic change

Question 5

How are mechanisms of cell injury classified?

Answer 5

According to causative agents and cellular targets

Question 6

What can causative agents be?

Answer 6

Physical, chemical, biological

Question 7

What are examples of physical causative agents?

Answer 7

Passive cell destruction, trauma and thermal injury, freezing, shearing forces

Question 8

What is the mechanism of chemical causative agents?

Answer 8

Toxic to specific metabolic pathways

Question 9

What are examples of biological causative agents?

Answer 9

Enzymes & toxins secreted by microorganisms, bacterial endotoxin, and viruses

Question 10

How do bacterial endotoxins cause cell injury?

Answer 10

Metabolic products/secretions are toxic to surrounding cells

Question 11

What is the effect of bacterial endotoxins?

Answer 11

They have a strong immune/inflammatory response, leading to damage to nearby cells.

Question 12

How do viruses cause cell injury?

Answer 12

They cause infected cells to physically rupture, resulting in local tissue damage from the host immune response.

Question 13

What can cellular targets be subdivided into?

Answer 13

Blockade of metabolic pathways, failure of membrane integrity, and DNA damage

Question 14

What are examples of cell injury due to blockade of metabolic pathways?

Answer 14

Cellular respiration, glucose deprivation, inhibition of protein synthesis, loss of growth factor/hormonal stimulus, ischemia & reperfusion injury

Question 15

What are examples of cell injury due to failure of membrane integrity?

Answer 15

Cell membrane damage, specific blockage of ion channels, failure of membrane ion pumps, free radical attack

Question 16

What may cause membrane damage?

Answer 16

Complement mediated cytolysis or perforin mediated cytolysis

Question 17

What may result from failure of membrane ion pumps?

Answer 17

Cells lysing

Question 18

What are mechanisms of cell injury due to DNA damage?

Answer 18

Single/double strand break, base alteration, or cross linkage

Question 19

What is a non-lethal cell injury due to DNA damage?

Answer 19

Inherited by daughter cells, leading to neoplastic transformation

Question 20

What are features of irreversible cell injury?

Answer 20

Irreversible mitochondrial dysfunction, profound membrane dysfunction

Question 21

What are examples of reversible cell injury?

Answer 21

Hydropic change, fatty change, autophagy

Question 22

What causes hydropic change?

Answer 22

Interference with membrane structure, interruption of energy supplies to membrane exchange systems, leading to dysregulated ion and water movement in/out of the cell

Question 23

What are features of hydropic change?

Answer 23

Pale and swollen cell cytoplasm, fluid accumulation

Question 24

How do cells that have undergone hydropic change survive for weeks?

Answer 24

No membrane and internal structure rupture, enough membrane function is present, allowing metabolic processes to function.

Question 25

Where are fatty changes mostly seen?

Answer 25

Liver, heart, kidney, which are cells with high lipid content/synthesis

Question 26

What is the mechanism for fatty change?

Answer 26

Uncoupling of lipid from protein metabolism, accumulation of triglycerides, leading to fatty globule formation in cells

Question 27

What are common causes of fatty changes/steatosis?

Answer 27

Toxins, chronic hypoxia, diabetes mellitus

Question 28

What is the pathogenesis of fatty change?

Answer 28

Increased mobilization of free fatty acids & cellular uptake, increased conversion of free fatty acids to triglycerides, decreased oxidation of triglycerides to acetyl-CoA, decreased lipid acceptor proteins preventing export of formed triglycerides

Question 29

What are causes of irreversible damage?

Answer 29

Free radicals, calcium ions, energy shortage, cell membrane dysfunction

Question 30

What is apoptosis?

Answer 30

Programmed/controlled cell death

Question 31

What is necrosis?

Answer 31

Uncontrolled cell death as a result of injury

Question 32

What are the types of necrosis?

Answer 32

Coagulative, colliquative, caseous, gangrene, fibrinoid necrosis, fat necrosis

Question 33

What are features of nuclear degeneration?

Answer 33

Karyopyknosis, karyorrhexis, karyolysis

Question 34

What is a pyknotic nucleus?

Answer 34

A small, condensed, and intensely haematoxylin stained/basophilic nucleus of a necrotic cell

Question 35

What is karyorrhexis?

Answer 35

Pyknotic nuclei fragmented into several particles

Question 36

What is karyolysis?

Answer 36

Complete breakdown of the nucleus

Question 37

What is the most common type of necrosis?

Answer 37

Coagulative necrosis

Question 38

What is coagulative necrosis?

Answer 38

Protein denaturation/coagulation followed by repair and regeneration

Question 39

What is colliquative/liquefactive necrosis?

Answer 39

Enzymatic digestion leading to cyst formation

Question 40

What is gangrene?

Answer 40

Necrosis with putrefaction of tissues, leading to black deposits of iron sulphide from degraded hemoglobin

Question 41

What are the causes of gangrene?

Answer 41

Bacterial infection, poor blood supply

Question 42

What is dry gangrene?

Answer 42

Gangrene affecting the toes

Question 43

What is wet gangrene?

Answer 43

Gangrene affecting the bowel

Question 44

What is fibrinoid necrosis?

Answer 44

Necrosis characterized by the deposition of fibrin-like protein in tissue

Question 45

What are apoptotic inhibitors?

Answer 45

Growth factors, extracellular matrix (ECM), sex steroids, some viral proteins

Question 46

What are apoptotic inducers?

Answer 46

Growth factor withdrawal, loss of ECM attachment, some viruses, free radicals, ionizing radiation, DNA damage, ligands binding death receptors

Question 47

What are the pathways of apoptosis?

Answer 47

Mitochondrial (intrinsic) pathway or death receptor (extrinsic) pathway

Question 48

What are the phases of apoptosis?

Answer 48

Activation of caspase 8 (initiator), cleaves executioner caspases (caspase 3 & 7), degradation of cellular components, caspases activate DNAse (fragments DNA), nucleus shrinks and fragments, cell shrinks, changes to membrane induce phagocytosis, if cell not phagocytosed, forms apoptotic body

Question 49

What are stimuli of the intrinsic pathway?

Answer 49

Growth factors, biochemical stress, DNA damage

Question 50

What does the intrinsic pathway of apoptosis cause?

Answer 50

Alterations in relative levels of pro and anti-apoptotic members of the Bcl-2 family

Question 51

What is Bcl-2?

Answer 51

A protein that inhibits apoptosis

Question 52

What is Bax?

Answer 52

A protein that stimulates apoptosis

Question 53

What is the extrinsic pathway of apoptosis?

Answer 53

Death receptors bind onto the cell surface, stimulating caspases

Question 54

What are death receptors?

Answer 54

TNF receptor 1, Fas

Question 55

What are causes of pathological apoptosis?

Answer 55

Radiation, chemotherapy, drugs

Question 56

What is asymmetric cell division?

Answer 56

One daughter cell progresses along the differentiation pathway and another replaces the parent cell

Question 57

What is the healing process?

Answer 57

Fibrin scab protects underlying skin, cells proliferate and spread as a thin sheet until the defect is covered, replaced from bottom up

Question 58

What is the process of repair?

Answer 58

Endothelial cells form vascular channels, fibroblasts proliferate and secrete collagen and other ECM proteins, combination of capillary loops and myofibroblasts leads to granulation tissue

Question 59

What are the consequences of large wound skin repair?

Answer 59

Loss of sweat glands and hair, keloid (raised) scar

Question 60

What stimulates skin repair of large wounds?

Answer 60

Cytokines and growth factors

Question 61

What factors affect repair?

Answer 61

Damage to fetus, old age, nutritional deficiencies, corticosteroids, disseminated malignancy, local ischemia, diabetes mellitus

Question 62

What is transmural infarction?

Answer 62

Myocardial infarction that involves full thickness of myocardium, extending through the muscularis propria to the serosa