week 1: acute inflammation

Question 1

define parenchyma

Answer 1

specialised cells of an organ

Question 2

define stroma

Answer 2

network supporting and holding together the specialised cells of an organ (collagen and fibroplasts)

Question 3

define endothelial cells

Answer 3

specialised cells lining the internal aspects of blood vessels

Question 4

define epithelial cells

Answer 4

cells that line organs, ducts, airways

Question 5

define pathophysiology

Answer 5

the physiology (process) behind pathological behaviours

Question 6

define pathogenesis/aetiology

Answer 6

the causal factors of a pathology
- smoking = emphysema

Question 7

define necrosis

Answer 7

death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply.

Question 8

define the 2 types of cell injury

Answer 8

reversible:
- cellular adaptation
- alterations in structure and function

irreversible
- lethal
- cell death
- necrosis

Question 9

what can reversible injury cause to a cell (DAHHM)

Answer 9

• atrophy: reduction in size and function
• hypertrophy: increasd in size and output
• hyperplasia: increase in cell number
• metaplasia: changes from one cell type to another cell type (notable in smokers epithelial cells)
• dysplasia: abnormal growth or development of cells or organs (most smokers develop dyplastic changes)

Question 10

how does loss of blood lead to cell death

Answer 10

• ischemia (blood flow is restricted to part of the body)
• decreased oxygen in the cells
• not enough o2 fo aerobic respiration
• decreased ATP due to anerobic glycolis increase
• lack of ATP to sodium potassium pump
• too many sodium/potassium ions enter cell
• water will follow sodium
• leads to loss of function

Question 11

how do injurous agents lead to cell death

Answer 11

• any injurous agents enters cell
• either damages plasma membrane or ATP production which allows ions into the cell
• increased calcium (damage to mitochondria)
• increased calcium (activate intracellular enzymes which damges cell membrane and production of phospholipids)
• cell death

Question 12

how do stressors (hypoxia, poison) lead to cell death

Answer 12

• increased production of reative oxygen species as well as o2 for ATP
• free radicals are produced
• ions grab onto electrons from other molecules and damage others
• dirupts cell membrane water and electrolytes
• cell damgage (mitochondria)
  -cell death

Question 13

what/how does hypoxia lead to cell death

Answer 13

hypoxia: preprogrammed cell death that happens all day everyday
- cell breaks down into small lipid enclosed packages
- therfore lysosomal enzymes (digestive enzymes) are contained

Question 14

can cell death cause inflammation

Answer 14

yes, except pre-programmed cell death
-un-programmed cell death releases digestive enzymes causing localised inflammation
-necosis follows this: it is the clean up process

Question 15

what is the main componenent of inflammation

Answer 15

blood:
- it contains all the neccessary elements
- eg. neutrophiuls
- lymphocytes
- monocytes

Question 16

define: nuetrophils, monocytes (macrophages), nuetrophils, T cells and B cells

Answer 16

• nuetrophils: first responders that phagocytose
• monocytes: turn into macrophges that become primary phagocytosers

lymphocytes: recruited when there is viruses/bacteria
- Killer T cells: kill and ingest
- Helper T cells: release chemical mediators driving response
- B cells: things that pump out antibodies

Question 17

what are the 2 types of immunity

Answer 17

innate: non-specific, no memory
- defence mechanism that you were born with

aquired: has specificity and memory
- cell mediated: T-cells recognise pathogens
- humoral: B cells produce antibodies mediators when presented with pathogen
- chemical mediators produce inflammatory response
- anti bodies lock onto pathogens
- destrohys pathogen by “revealing it to toher cells, cause blood protiens to lock onto pathogen, or covers all receptor cites of pathogen

Question 18

define accute inflammation

Answer 18

an immediate, adaptive response with limited specificity caused by several noxious stimuli, such as infection and tissue damage

Question 19

what are the 2 phases of accute inflammation

Answer 19

vascular
cellular

Question 20

steps of vascular inflammation

Answer 20

• chgemical mediatos released by phagocytosis
• vasoconstricton
• vasodilation (nitroxcide relaxes smooth muscle)
• hyperaemia (increased blood to area)
• increase in hydrostatic pressure
• increase of fluid/plasma loss (transudate)
• increased concentation of cells
• increased blood flow/ blood slows becuase of high cellular concentration

Question 21

steps of cellular inflammation

Answer 21

• increased activation of endothelial cells
• inceased adhesiveness
• WBC’s marginate and aggregate at injuy site
• gaps develop between endothelial cells
• diapedisis: WBC moving across chemical gradient
• transudate: plasma moveing across
• exudate: cells moving across
• edema occurs (swelling)
• phagocytosis of offending agent (nuetrophils, monocytes-macrophages)
• release of cytokines (MMP’s) for further destruction, also destructs surrounding material (not much in acute)
• if it is viral/bacterial T-cells and B-cells will move in (not regular for acute inflamm)

Question 22

what are the outcomes of acute inflammation

Answer 22

• slight tissue damge but removal of agent (back to normal)
• siubstantial tissue damage, or in non regenerative tissue, or lots of fibrin exudate (healing by scarring)
• necrosis + bacterial/fungal inffection (formulationf of granulation tissue, absess)
• tissue damge and persistance of agent (chronic inflammation)