Bio Factsheet

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The Biology of a nail in the foot“It doesn’t mention anything about nails ib the foot on my Specification, why should I bother reading this Factsheet?”

Three reasons:1. It’s a brilliant synoptic topic, bringing in bodily defences, clotting and the immune response2. It’s an example of an applied topic – and application questions can sometimes be tricky and time-consuming, as many AQA candidates

discovered in the Jan 2010 papers3. It’s really interesting stuff and a good interview riposte when the Admissions Officer kindly enquires “Tell us something interesting

that you’ve learned in Biology recently”

You cut your foot on a nail and your foot begins to bleed. What happens next?

Your body tries to stop the loss of blood (Fig.1)

5. The fibrin forms a mesh that traps red blood cells,forming a clot which stops blood loss

bacteria

red blood cells

blood platelets

epidermisdermiscapillary

white blood cell

red blood cellplatelet

1. Blood comes into contact with collagen withinthe wall of the damaged blood vessel. Thiscauses platelets to become activated and theycollect and form a plug at the wound site1

2

2. The platelets disintegrate and release severalclotting factors including thromboplastin, asdoes the damaged tissue

thromboplastin(from damagedtissue and platelets)

Ca2+ and vitaminK (in the plasma)

3. In the presence of calcium ions, thromboplastinstimulates the conversion of inactive prothrombinto the enzyme thrombin

capillary wall

3

fibrin

fibrin meshtrapping bloodcells

platelets stickto wall andeach otherforming aplatelet plug

4. Thrombin catalyses the hydrolysis of four peptidebonds from soluble fibrinogen, allowing itspolymerisation into long, insoluble strands of fibrin

5

Fig 1

thromboplastin + Ca2+

prothrombin thrombin

thrombinsoluble fibrinogen insoluble fibrin

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AnswersCan’t produce thrombin;blood does not clot;bleeding continues for longer;more time for entry of pathogens;

Dealing with pathogensThe bacteria that entered the bloodstream from the nail will releasechemicals that attract phagocytic white cells, the first of which areneutrophils. The neutrophils stick to the walls of the blood vesselsand then squeeze between the endothelial cells The phagocytesuse chemotaxis to move towards the invading bacteria and destroythem via phagocytosis (Fig.2).

Fig 2. Phagocytosis

Typical Exam QuestionSome people are unable to produce factor VIII, one of the clottingfactors. Suggest why this poses a risk to their health (3)

Despite these attempts to eliminate the bacteria, it is likely that some bacteria will get carried to other parts of the body in the lymph orblood. Bacteria in the lymph will encounter yet more macrophages when the lymph passes through the lymph nodes. Those that aredistributed in the blood will run into macrophages when the blood passes through the spleen and liver.

Active immunityThe antigens on the surface of the bacteria will be recognised as foreign (non-self) and this stimulates B-lymphocytes to manufactureantibodies. Antibodies are proteins that bind to the antigens on the bacteria., enabling the phagocytes to recognise them as foreigninvaders.

If, in future, these same species of bacteria enter the body again, the person’s response to this second infection will be even faster thanthe response to the first infection. This is because the memory (B)-cells formed in the previous attack will already be present and as soonas the bacteria are recognized the memory cells will divide rapidly to form plasma cells which produce antibodies more quickly and ingreater numbers than the first time.

InflammationThe area around the cut also becomes inflamed – red and sore. This is known as the inflammatory response and helps to kill the bacteriaand prevent the spread of infection.

Inflammatory response• Damaged white blood cells and mast cells in the connective tissue release chemicals such as histamine.

• Histamine causes dilation of arterioles and thus increases the blood flow in the surrounding capillaries

• Cells in the capillary walls separate slightly making the capillaries leaky

• Plasma fluid, antibodies and white blood cells leak out into the tissue causing swelling (oedema)

• Thus the number of white blood cells in the area increases and more bacteria are attacked

Neutrophils arrive first and engulf between 5-20 bacteria before dying. Macrophages arrive next and these bigger, longer-lived cells arecapable of killing many more bacteria. Over the course of the next few days the area will become filled with dead cells, mainly neutrophilswhich form a whitish, thick fluid or pus. The pus may leak out of the wound or be gradually reabsorbed into the surrounding tissue.

1. Bacteria become attached tothe neutrophil

2. The neutrophilengulfs thebacteria

3. Bacteria are enclosed in a vacuole.Lysosomes fuse with the vacuole andrelease digestive enzymes that destroy thebacteria

Watch a neutrophil in action!Type in neutrophil phagocytosis in YouTubeto see the chase

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AntibodiesEach B-cell can only produce one type of antibody. Each antibody is only capable of binding to one specific antigen. How then do we copewith the fact that there are hundreds of thousands of different types of pathogen, each of which has several different antigens on theirsurface?

The answer is that, at an early stage in the development of the embryo, 100 million different B cells are produced in the bone marrow. EachB cell divides rapidly to create a clone of cells that provide the baby with an immune system capable of responding rapidly and specificallyto millions of antigens that may enter the body over the lifetime of the person.

The structure of antibodiesAntibodies are proteins and it is important to understand that it is the protein nature of antibodies that enables us to produce theenormous range of antibody required over the course of our lives.

binding site attaches to the antigen. The part ofthe antibody molecule incorporating the bindingsite is often called the variable region becausedifferent antibodies have different amino acidsequences, hence different shapes. It is thesedifferences in 3D shape that give the specificitybetween antibody and antigen. The relationshipbetween the variable region on the antibody andthe antigen on the pathogen is similar to thatbetween an enzyme’s active site and the enzyme’ssubstrate

binding site

Typical Exam QuestionThe graph shows the concentration of antibodies in a student’sblood following a first infection by a type of bacteria.

disulphide bridge maintains the shape(tertiary structure) of the molecule

hinge region allows the molecule tobend and bind with more than onepathogen

constant region holds the polypeptide chainstogether and maintains the quaternary structure

Fig 3 Antibody structure

(a) Name the type of cell that produces antibodies (1).(b) Explain why there is a delay between the infection and the

appearance of antibodies in the blood (2)(c) On day 35 the student suffered a second infection of the same

pathogen. Draw a curve to show the expected concentration ofantibodies in the blood following this infection. Explain the shapeof your curve (4)

0 10 20 30 40 50 60 70 80 90 100

concentrationof antibodies/arbitary units

20

40

60

80

100

120

140

time/days since first infection

020406080

100120140

0102030405060708090100time/days since first infection

concentrationof antibodies/arbitary units

rise starts between day 36-40;rise is steeper and rises higher (50au) than first response;concentration declines more slowly/with less steep gradient;immunological memory / memory cells are present;so no need for antigen presentation;no need for clonal selection;only clonal expansion required ;

Markscheme(a)B cell/ B lymphocyte/ plasma cell;

(b)time taken for antigen presentation;protein synthesis takes time;cloning of antibodies takes time;there are no memory cells because it is a first infection;

(c)

0

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Acknowledgements:This Factsheet was researched and written by Kevin Byrne.Curriculum Press, Bank House, 105 King Street, Wellington, Shropshire,TF1 1NU.Bio Factsheets may be copied free of charge by teaching staff or students,provided that their school is a registered subscriber. No part of theseFactsheets may be reproduced, stored in a retrieval system, or transmitted,in any other form or by any other means, without the prior permission ofthe publisher. ISSN 1351-5136

Practice Questions1. The diagram shows the main stages in blood clotting.

T lymphocytesThere are two types of T lymphocyte:

• T helper cells and• T killer cells.

T helper cells help B cells to divide and help phagocytes kill the bacteria effectively. T killer cells recognize and destroy any cells thathave become infected with the bacteria. When a cell becomes infected by the bacteria the cell displays a fragment of the bacterialantigen on its cell surface. T killer cells bind to the antigen and clone themselves. They then release enzymes that digest parts of thesurface membrane of the infected cell. Water and ions enter the infected cell which then bursts (lysis). The bacteria are thus releasedand can be labeled by antibodies, flagging them up as targets for the macrophages.

thromboplastin releasedfrom platelets

....................... ions and plasma enzymes

inactive...........................

active...........................

soluble...........................

insoluble...........................

blood clot forms

Complete the boxes to show the names of the substancesinvolved (5)

2. State two structural features of an antibody molecule and explainhow each feature helps the antibody to perform its function (4).

3. The graph below shows the concentration of antibodies in theblood following a first infection by a bacterial pathogen on day0 and a second infection of the same bacteria on day 35.

Explain the shape of the primary and secondary response shown(6)

concentrationof antibodies/arbitary units

time/days since first infection

20

40

60

80

00 10 20 30 40 50

Markschemes1.Calcium;

Prothrombin;Thrombin;FibrinogenFibrin;

2.binding site;attaches to antigen/ has complementary shape to the antigen;.

disulphide bridge; maintains the shape (tertiary structure) of the molecule;

constant region;holds the polypeptide chains together/ maintains the quaternarystructure;

hinge region;allows the molecule to bend and bind with more than onepathogen;

3.Days 0-5 = time taken for antigen presentation;protein synthesis;cloning of antibodies;there are no memory cells because it is a first infection;secondary response is faster;and greater;because of immunological memory / memory cells are present;so no need for antigen presentation at second infection;no need for clonal selection;only clonal expansion required;