1. WELCOME BACK  How much revision have you done over the xmas holiday?
You will be sitting an exam next Monday.
The topics to be examined include:
Lungs and Lung Disease
Heart and Heart Disease
Immunity
Cells (organelles, Microscopes and Centrifugation)
Enzymes
How much revision have you done over the xmas holiday?
Write down what you have done to revise.

2. What are we trying to find out?
Lesson Objectives
What are we trying to find out?
LUNGS AND LUNG DISEASE
How does fibrosis affect lung function?

3. Tuberculosis

5. Tuberculosis
Link
Results in fibrosis or scarring of the lungs…

6. Fibrosis
Scar tissue is less elastic and thicker than normal lung tissue.
Concentration gradient between alveoli and capillaries
Diffusion distance between alveoli and capillaries
Explain the consequences of scar tissue on these features.
Ability to breathe in and out.

7. What are we trying to find out?
Lesson Objectives
What are we trying to find out?
LUNGS AND LUNG DISEASE
How does fibrosis affect lung function?

8. What are we trying to find out? HEART AND HEART DISEASE
Lesson Objectives
What are we trying to find out?
HEART AND HEART DISEASE
What are the risk factors for coronary heart disease?
How does an atheroma cause a heart attack?
How is blood flow related to changes in pressure?
How do we calculate heart rate from graphs?

9. Create a Spider Diagram.
What are the risk factors which increase your chances of suffering coronary heart disease?

10. Coronary Heart Disease
High blood pressure
Genetics
High Saturated fat
High Salt
High Cholesterol
Smoking
Lack of Exercise/Activity
Gender

11. Artery

12. Atheroma Damage can occur to the artery through high blood pressure.
White blood cells and LDL-cholesterol from the blood can accumulate and clump together under the lining to form fatty streaks.

13. Atheroma

14. Atherosclerosis
Over time, more white blood cells and LDL-cholesterol and fat get deposited in the wall.
This deposit enlarges and hardens to form a fibrous plaque known as an atheroma.

15. Atherosclerosis
Eventually, the artery becomes so narrow that blood flow is constricted.
Blood pressure further increases.

16. Thrombosis Atheroma’s can lead to damage of the inner artery wall.
The plaque can rupture through the weakened wall, creating a rough surface.
Platelets and fibrin (a protein involved in clotting) accumulate at the site forming a clot (thrombus).

18. Thrombosis
The blood clot (thrombus) can completely block blood flow in an artery.

22. The cardiac cycle SL valves close SL valves open AV valves close
AV valves open

25. What are we trying to find out?
Lesson Objectives
What are we trying to find out?
IMMUNITY
What are antigens?
How are antibodies produced?
What are some of the disadvantages of giving a vaccination?
How can we diagnose the presence of an antigen in a patients blood stream?

26. Antigens An antigen is a protein which stimulates an immune response.
They could form part of the membrane or cell wall of a pathogen or cancer cell. They could be a toxin.

27. B Cell Activation
When a pathogen invades, the specific B Cell which has a shape to match the antigens on the pathogen binds to the pathogen.

28. B Cell Activation
The B Cell is activated by a T Helper Cell to start dividing by mitosis to form a clone army!

29. B Cell Activation The B Cell develops into 2 types of cell:
Plasma Cells
Memory Cells

30. B Cell Activation
Plasma Cells secrete specific antibody which attaches to the antigens and destroys the pathogen.
As antibody deals with pathogens within the body fluids, we call the response humoral immunity.

31. B Cell Activation
The antibodies also make the pathogen more attractive to phagocytes.

32. B Cell Activation
The memory cells will linger around the body for the rest of the individuals life.
They can produce a faster response should the person become infected again…

34. 34/5

40. What are we trying to find out?
Lesson Objectives
What are we trying to find out?
ENZYMES
How do enzymes work?
What are the differences between competitive and non-competitive inhibitors?

41. How do catalysts like enzymes work?
What are enzymes?
Enzymes are biological catalysts – they speed up the chemical reactions that take place inside all cells.

42. What are enzymes made of?
How do catalysts like enzymes work?
What are enzymes made of?
Enzymes are tertiary protein structures made up of a chain of amino acids which has been folded into a specific 3D shape.

43. Sucrose + Water  Glucose + Fructose
How do catalysts like enzymes work?
Activation Energy
Sucrose + Water  Glucose + Fructose
This hydrolysis reaction will take place.
However, it will be very slow.
For the reaction to take place, the following requirements must take place:
There must be collisions between the sucrose and water molecules. This alters atoms and bonds to form the products.
These collisions must have enough energy to activate the reaction. This is the activation energy.

44. How do catalysts like enzymes work?

45. How do catalysts like enzymes work?
Enzymes speed up chemical reactions by lowering the activation energy.
This means that chemical reactions can happen at lower temperatures (37oC).

46. How do catalysts like enzymes work?

47. Why are enzymes so specific?
What do enzymes look like?
Why are enzymes so specific?
Enzymes are very specific about which reactions they catalyse. Only molecules with exactly the right shape will bind to the enzyme and react.
These are the reactant, or substrate, molecules.
The part of the enzyme to which the reactant binds is called the active site.

48. What do enzymes look like?

49. What happens at the active site?
What do enzymes look like?
What happens at the active site? + + ↔ ↔
enzyme
reactant +
enzyme ↔
enzyme-substrate complex ↔ +
products

50. What are the different models of enzyme action?

51. What are the different models of enzyme action?

52. What are the different models of enzyme action?
Induced Fit
Link

53. Lock and key hypothesis
53/5
Lock and key hypothesis

54. 54/5
Induced fit model

55. Competitive Inhibitors
Competitive -These bind to the active site, blocking it , preventing the formation of E-S complexes.
They are often similar in shape to the substrate.
Sometimes molecules with a similar shape attach to the active site. If these are present in the same solution they compete for the active site. They block it. So fewer enznymes are available for a reaction and the rate reduces.

56. The inhibitor does not attach permanently to the A.S
Inhibition caused by a competitive inhibitor can often be reversed by the addition of further substrate.
High substrate concentrations allow the substrate to occupy the active site reducing the chances of the inhibitor binding.
Add graph here

58. Non-competitive Inhibitors
These bind to the enzyme away from the active site, but still cause the shape of the active site to change, this stops the substrate from binding.
Therefore, the enzyme cannot function.
As the substrate and enzyme are not competing for the same site, an increase in substrate does not decrease the effect of the inhibitor.
Add diagram, page 36 figure 2 is good and could be copied.
G.Ray 2009

59. Increasing the substrate concentration has no effect on this type of inhibition as it does nothing to prevent the inhibitor from binding away to the active site.
Add graph here, any animations. May remain permanently attached therefore, the enzyme is effectively destroyed.
G.Ray 2009