W1- Cell Injury

Question 1

Who invented the microscope?

Answer 1

Robert Hooke

Question 2

What is pathology?

Answer 2

The study of suffering/disease

Question 3

What are the 7 causes of cell injury?

Answer 3

Hypoxia, physical agents (trauma, heat, cold, radiation), chemical agents and drugs (positions, alcohol), microorganisms, immune mechanisms, dietary insufficiencies/excess, genetic abnormalities (IEM)

Question 4

What is the difference between hypoxia and ischemia?

Answer 4

Hypoxia= lack of adequate 02 supply, Ischemia= lack of adequate blood supply

Question 5

What are the 4 types of hypoxia? Explain each

Answer 5

Hypoaxaemic, anaemic, ischaemic, histiocytic

Question 6

What is a hypersensitivity reaction? Give an example

Answer 6

Host tissue is injured but overly vigorous IR occurs e.g. Hives

Question 7

What components of the cell can be targeted during cell injury?

Answer 7

Cell membrane and organelle membranes, nucleus, proteins, MT

Question 8

What are the two most common causes of cell injury?

Answer 8

Hypoxia and ischemia

Question 9

Explain what happens during reversible hypoxia.

Answer 9

Less O2, decreased ATP production from oxidative P, when less than 5-10% loss of Na+/K+ pump activity, Na+ conc rises IC, awaited follows, cell swells, Ca2+ enters too and damages. Glycolysis provides ATP but produces lactic acid decreasing pH, chromatin clumps, ribosomes detach from ER and protein synthesis stopped. Heat shock response

Question 10

Explain irreversible hypoxic injury.

Answer 10

Not sure at what point it occurs. Massive influx of Ca2+ and release from SR, phospholipases damage p.m., proteases damage cytoskeleton and membrane proteins, ATPase reduce ATP, endonucleases cause chromatin clumping. ER and organelles swell, enzymes leak out of lysosomes, p.m. blebbing, cell dies- blew may burst

Question 11

Free radicals are….

Name the 3 most biologically important.

Answer 11

Reactive oxygen species- single unpaired e- in outer orbital, hydroxyl, superoxide, hydrogen peroxide

Question 12

When are free radicals produced?

Answer 12

When radiation loses water- Fenton reaction, Haber-Weiss reaction, during normal metabolic reactions in the MT

Question 13

What cellular structures are damaged by free radicals?

Answer 13

Lipids in cell membranes- cause lipid peroxidation- chain reaction of more free radicals. Attack proteins, carbs and DNA too

Question 14

How does the body defend against free radicals?

Answer 14

Anti-oxidant system- enzymes (SOD and catalase), free radical scavengers (vitamins A,C,E), storage proteins. Many decay spontaneously

Question 15

What may cause ischemia reperfusion injury?

Answer 15

02 free radical production during reoxygenation, increased neutrophils causing increased inflammation, delivery of complement and activation of complement pathway

Question 16

Why is cyanide toxic?

Answer 16

It binds to MT cytochrome oxidase and blocks oxidative P

Question 17

Why are heat-shock proteins protective? Give an example

Answer 17

They mend misfolded proteins by unfoldases or chaperonins e.g. Ubiquitin

Question 18

What changes can be seen by LM and EM in injured cells?

Answer 18

Cytoplasmic, nuclear, intracellular accumulations (see slide 29)

Question 19

Define oncosis

Answer 19

Cell death with swelling, prior to death. ATP independent.

Question 20

Define necrosis

Answer 20

Morphologic changes that occur after a cell has died. ATP independent.

Question 21

Define apoptosis

Answer 21

Programmed cell death with cellular shrinkage. Activated enzymes grade own DNA and proteins. ATP dependent. Quick

Question 22

Microscopic changes seen in apoptosis

Answer 22

Membrane integrity preserved. Nuclear fragmentation and chromatin condensation. Apoptosis bodies

Question 23

Microscopic changes seen in oncosis and necrosis

Answer 23

P.m ruptures, cell and MT swelling. P.m blebbing in oncosis

Question 24

What are the two main types of necrosis and the two other types?

Answer 24

Coagulative (protein desaturation), liquefactive (enzyme release). Caseous and fat necrosis

Question 25

What is dry and wet gangrene?

Answer 25

Dry gangrene- air dries e.g umbilical cord, wet- infection

Question 26

Define infarct and when it occurs

Answer 26

=ischemic necrosis. Red (haemorhhagic) and white (No blood, blocked artery).

Question 27

Which 3 molecules are released by injured cells?

Answer 27

K+, enzymes, Mb

Question 28

What are the 3 phases of apoptosis?

Answer 28

Initiation, execution, degradation and phagocytosis

Question 29

What does p53 do?

Answer 29

Tumour suppressor- mediates apoptosis in response to DNA damage

Question 30

Is inflammation seen in apoptosis and oncosis?

Answer 30

Yes in oncosis (release of proteolysis enzymes), no in apoptosis.