Lecture 2 - Acute Inflammation

Question 1

Effects of cellular injury?

Answer 1

loss of energy, membrane damage (Mt, lysozome, cell wall), protein & Dna breakdown (increased calcium and reactive oxygen species)

Question 2

Causes of ATP depletion?

Answer 2

lack of oxygen, Mt damage, damage to enzymes

Question 3

ATP depletion leads to?

Answer 3

decreased repairing enzymes, decreased ion channels (Na build up draws water causing swelling, Ca build up activates destructive enzymes), decreased protein synthesis

Question 4

Plasma membrane damage results in?

Answer 4

loss of cellular contents, osmotic balance, influx of fluid & ions, loss of proteins enzymes co-enzymes and ribo-nucleic acids

Question 5

Autolysis?

Answer 5

Digestion of cellular components by leaked lysozymes

Question 6

Mitochondrial membrane damage results in?

Answer 6

non-selective high-conductance chanels form in inner membrane, removes TMP, cyt C leaks into cytosol prompting apotosis

Question 7

Increased cytosolic Ca effects?

Answer 7

increased ATPase, phospholipase and protease (damaging cell membrane), and endonuclease

Question 8

Heat shock factors?

Answer 8

Stress or injury activate these transcription factors that form heat shock proteins assist the repair of cellular proteins

Question 9

Methods of adaptation?

Answer 9

hyperplasia, hypertrophy, atrophy, metaplasia

Question 10

Characteristics of Necrosis?

Answer 10

passive cell death from overwhelming damage, autolysis, cytosolic leak leading to inflammatory response

Question 11

Apoptosis characteristics?

Answer 11

When cell has enough energy to commit sepuku, phagocytosis by macrophages or neighbouring cells, nucleus shrinks, membrane blebs, cascade of upstream caspases leading to executioner caspases

Question 12

Triggers of Inflammation?

Answer 12

Infections, trauma, physical and chemical agents, necrosis, foreign bodies, immune response

Question 13

Acute inflammation steps?

Answer 13

trigger, blood flow & permeability changes, change in endothelial signalling and gene expression, change in neutrophil signalling and gene expression, neutrophil activation, survival, function, death, inflammation subsides (acute) or recruits other leukocytes (chronic)

Question 14

Increased processes in inflammed endothelial cells?

Answer 14

Cell-adhesion molecules, anti-apoptosis molecules, cytokines and chemokines, coagulation factors, pro-angiogenesis factors, signalling molecules

Question 15

Decreased processes in inflammed endothelial cells?

Answer 15

Cytokine stabilizers, signalling molecules

Question 16

Blood flow and permeability changes?

Answer 16

increased flow (hyperaemia), loss of fluid and protein (exudation), fibrinous exudate and tissue oedema, stasis and leukocyte margination in post-capillary venules

Question 17

Neutrophils activated by?

Answer 17

endothelial cell surface molecules, interleukin 1, tumour necrosis factor, bacterial factors, chemotactic factors