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Biology IB HL > 6.3 Disease Defences > Flashcards

6.3 Disease Defences Flashcards

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1
Q

What is the first line of defence?

A

The first line of defence against infectious disease are the surface barriers that prevent the entry of pathogens into the body

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2
Q

What are examples of the first line of defence? 2

A

These surface barriers include both the intact skin and mucous membranes

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3
Q

What does the skin protect?

A

Protects external structures when intact (outer body areas)

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4
Q

What is the physical barrier part of the skin?

A

Consists of a dry, thick and tough region composed predominantly of dead surface cells

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5
Q

What is the chemical barrier of the skin?

A

Contains biochemical defence agents (sebaceous glands secrete chemicals and enzymes which inhibit microbial growth on skin)

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6
Q

What does the skin secrete?

A

The skin also secretes lactic acid and fatty acids to lower the pH (skin pH is roughly ~ 5.6 – 6.4 depending on body region)

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7
Q

What do mucous membranes protect?

A

Protects internal structures (i.e. externally accessible cavities and tubes – such as the trachea, oesophagus and urethra)

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8
Q

What is the PHYSICAL part of the mucous membranes?

A

Consists of a thin region of living surface cells that release fluids to wash away pathogens (mucus, saliva, tears, etc.)

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9
Q

What is the CHEMICAL part of the mucous membranes?

A

Contains biochemical defence agents (secretions contain lysozyme which can destroy cell walls and cause cell lysis)

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10
Q

What may mucous membranes have, to further aid pathogen removal?

A

Mucous membranes may be ciliated to aid in the removal of pathogens (along with physical actions such as coughing / sneezing)

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11
Q

What is clotting?

A

Clotting (haemostasis) is the mechanism by which broken blood vessels are repaired when damaged

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12
Q

What is the role of clotting?

A

Clotting functions to prevent blood loss from the body and limit pathogenic access to the bloodstream when the skin is broken

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13
Q

What are the two key components of a blood clot?

A

platelets and insoluble fibrin strands

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14
Q

What is the role of platelets in blood clotting?

A

Platelets undergo a structural change when activated to form a sticky plug at the damaged region (PRIMARY haemostasis)

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15
Q

What is the role of fibrin strands in blood clotting?

A

Fibrin strands form an insoluble mesh of fibres that trap blood cells at the site of damage (SECONDARY haemostasis)

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16
Q

What set of reactions are involved in blood clotting?

A

The process by which blood clots are formed involves a complex set of reactions collectively called the coagulation cascade

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17
Q

What is the coagulation cascade triggered by?

A

This cascade is stimulated by clotting factors released from damaged cells (extrinsic pathway) and platelets (intrinsic pathway)

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18
Q
  1. Clotting - What do clotting factors stimulate, in terms of platelets?
A

Clotting factors cause platelets to become sticky and adhere to the damaged region to form a solid plug

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19
Q
  1. Clotting - What do clotting factors stimulate, in terms of physical changes?
A

These factors also initiate localised vasoconstriction to reduce blood flow through the damaged region

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20
Q
  1. Clotting - What do clotting factors stimulate, in terms of a conversion?
A

Additionally, clotting factors trigger the conversion of the inactive zymogen prothrombin into the activated enzyme thrombin

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21
Q
  1. Clotting - What does thrombin catalyse?
A

Thrombin in turn catalyses the conversion of the soluble plasma protein fibrinogen into an insolube fibrous form called fibrin

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22
Q
  1. Clotting - What do fibrin strands form?
A

The fibrin strands form a mesh of fibres around the platelet plug and traps blood cells to form a temporary clot

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23
Q
  1. Clotting - What happens once the area has healed?
A

When the damaged region is completely repaired, an enzyme (plasmin) is activated to dissolve the clot

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24
Q

Where can the concept of clotting be applied to, i.e. another part of the syllabus?

A

Coronary thrombosis is the formation of a clot within the blood vessels that supply and sustain the heart tissue (coronary arteries)

Occlusion of a coronary artery by a blood clot may lead to an acute myocardial infarction (heart attack)

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25
Q

Explain the process of atherosclerosis and coronary thrombosis
(better flashcard i.e. process broken down in 6.2. blood system flashcards)

A

Blood clots form in coronary arteries when the vessels are damaged as a result of the deposition of cholesterol (atherosclerosis)

Atheromas (fatty deposits) develop in the arteries and significantly reduce the diameter of the lumen (stenosis)
The restricted blood flow increases pressure in the artery, leading to damage to the arterial wall (from shear stress)
The damaged region is repaired with fibrous tissue which significantly reduces the elasticity of the vessel wall
As the smooth lining of the artery is progressively degraded, lesions form called atherosclerotic plaques
If the plaque ruptures, blood clotting is triggered, forming a thrombus that restricts blood flow
If the thrombus is dislodged it becomes an embolus and can cause a blockage in a smaller arteriole

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26
Q

What is the second line of defence?

A

The second line of defence against infectious disease is the innate immune system, which is non-specific in its response

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27
Q

What is the PRINCIPLE component of the second line of defence?

A

A principle component of this line of defence are phagocytic white blood cells that engulf and digest foreign bodies

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28
Q

What are OTHER components of the second line of defence?

A

Other components of the innate immune system include inflammation, fever and antimicrobial chemicals (complement proteins)

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29
Q

What are the key properties fo the innate immune system?

A

It does not differentiate between different types of pathogens (non-specific)
It responds to an infection the same way every time (non-adaptive)

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30
Q

What is phagocytosis?

A

Phagocytosis is the process by which solid materials (such as pathogens) are ingested by a cell (i.e. cell ‘eating’ via endocytosis)

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31
Q
  1. Phagocytosis - How is the process of phagocytosis initiated?
A

Phagocytic leukocytes circulate in the blood and move into the body tissue (extravasation) in response to infection

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32
Q
  1. Phagocytosis - what does damaged tissue release and what does this trigger?
A

Damaged tissues release chemicals (e.g. histamine) which draw white blood cells to the site of infection (via chemotaxis)

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33
Q
  1. Phagocytosis - How is the pathogen surrounded?
A

Pathogens are engulfed when cellular extensions (pseudopodia) surround the pathogen and then fuse to form an internal vesicle

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34
Q
  1. Phagocytosis - What fuses with the phagosome?
A

The vesicle is then fused to a lysosome (forming a phagolysosome) and the pathogen is digested

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35
Q
  1. Phagocytosis - what may be done with the antigen of the digested pathogen?
A

Pathogen fragments (antigens) may be presented on the surface of the phagocyte in order to stimulate the third line of defence

36
Q

What is the third line of defence?

A

The third line of defence against infectious disease is the adaptive immune system, which is specific in its response

37
Q

Can the 3rd line of defence differentiate between particular pathogens?

A

YES
It can differentiate between particular pathogens and target a response that is specific to a given pathogen

38
Q

Is the 3rd line of defence involved in immunological memory?

A

YES
It can respond rapidly upon re-exposure to a specific pathogen, preventing symptoms from developing (immunological memory)

39
Q

What is the adaptive immune system coordinated by?

A

The adaptive immune system is coordinated by lymphocytes (a class of leukocyte) and results in the production of antibodies

40
Q

What are B lymphocytes?

A

B lymphocytes (B cells) are antibody-producing cells that recognise and target a particular pathogen fragment (antigen)

41
Q

What are helper T lymphocytes?

A

Helper T lymphocytes (TH cells) are regulator cells that release chemicals (cytokines) to activate specific B lymphocytes

42
Q

What may some phagocytic leukocytes present?

A

When phagocytic leukocytes engulf a pathogen, some will present the digested fragments (antigens) on their surface

43
Q
  1. Antibody Production - What is the role of the antigen-presenting cells (APC)?
A

These antigen-presenting cells (dendritic cells) migrate to the lymph nodes and activate specific helper T lymphocytes

44
Q
  1. Antibody Production - what do the helper T cells release?
A

The helper T cells then release cytokines to activate the particular B cell capable of producing antibodies specific to the antigen

45
Q
  1. Antibody Production - what happens to the activated B cell?
A

The activated B cell will divide and differentiate to form short-lived plasma cells that produce high amounts of specific antibody

46
Q
  1. Antibody Production - What will antibodies target?
A

Antibodies will target their specific antigen, enhancing the capacity of the immune system to recognise and destroy the pathogen

47
Q
  1. Antibody Production - What may some activated B cells transform into?
A

A small proportion of activated B cell (and activated TH cell) will develop into memory cells to provide long-lasting immunity

48
Q

What is an antigen?

A

Antigen: An antigen is a substance that the body recognises as foreign and that will elicit an immune response

49
Q

What is an antibody?

A

Antibody: An antibody is a protein produced by B lymphocytes (and plasma cells) that is specific to a given antigen

50
Q

What are antibodies made of?

A

Antibodies are made of 4 polypeptide chains that are joined together by disulphide bonds to form Y-shaped molecules

51
Q

Where does the antigen bind to? (antibodies)

A

The ends of the arms are where the antigen binds – these areas are called the variable regions and differ between antibodies

52
Q

Apart from the variable region (where antigen binds), is the rest of the antibody structure different?

A

NO
The rest of the molecule is constant across all antibodies and serves as a recognition site for the immune system (opsonisation)

53
Q

What can antibody-antigen interaction be compared to?

A

Each type of antibody recognises a unique antigen, making antigen-antibody interactions specific (like enzymes and substrates)

54
Q

What are antibiotics?

A

Antibiotics are compounds that kill or inhibit the growth of microbes (specifically bacteria) by targeting prokaryotic metabolism

55
Q

What are 3 metabolic features that may be targeted by antibiotics?

A

Metabolic features that may be targeted by antibiotics include key enzymes, 70S ribosomes and components of the cell wall

56
Q

Do antibiotics target both eu- and prokaryotic cells? Why?

A

Because eukaryotic cells do not possess these features, antibiotics will target the pathogenic bacteria and not the infected host

57
Q

In what two general ways may an antibiotic kill invading bacteria?

A

Antibiotics may either kill the invading bacteria (bactericidal) or suppress its potential to reproduce (bacteriostatic)

58
Q

What is the mode of infection for viruses?

A

Viruses do not possess a metabolism (they are not alive) and instead take over the cellular machinery of infected host cells

59
Q

Therefore, are antibiotics effective for viruses?

A

NO!!!
As such, they cannot be treated with antibiotics and must instead be treated with specific antiviral agents

60
Q

What do antiviral treatments target?

A

Antiviral treatments target features specific to viruses (e.g. viral enzymes like reverse transcriptase or components of the capsid)

61
Q

What two types of antibiotics may there be?

A

Antibiotics can be narrow spectrum (effective against specific bacteria) or broad spectrum (effective against many bacteria)

62
Q

When was the first antibiotic discovered?

A

Since the discovery of the first antibiotic in 1928, antibiotic compounds have been used to treat a variety of bacterial infections

63
Q

What have some strains of bacteria developed?

A

Some strains of bacteria have evolved with genes that confer resistance to antibiotics and some strains have multiple resistance

64
Q

How may genes in bacteria confer resistance?

A

Genes may confer resistance by encoding traits that degrade the antibiotic, block its entry, increase its removal or alter the target

65
Q

Why is antibiotic resistance possible in bacteria?

A

Because bacteria reproduce at a rapid rate, resistant strains of bacteria can proliferate very quickly following the initial mutation

66
Q

How can the resistant strain be passed on?

A

Additionally, resistant strains can pass resistance genes to susceptible strains via bacterial conjugation (horizontal gene transfer)
+ binary fission

67
Q

What are three factors that are causing an increase in the prevalance of resistant bacterial strains?

A
  1. Antibiotics are often over-prescribed (particularly broad-spectrum drugs) or misused (e.g. given to treat a viral infection)
  2. Many antibiotics are freely available without a prescription and certain antibiotics are commonly included in livestock feed
  3. Multi-drug resistant bacteria are especially common in hospitals (i.e. nosocomial infections) where antibiotic use is high
68
Q

What is an example of an antibiotic-resistant strain?

A

An example of an antibiotic-resistant strain of bacteria is Golden Staph (MRSA – Methicillin Resistant Staphylococcus aureus)

69
Q

Who found the first chemical compound?

A

The first chemical compound found to have antibiotic properties was penicillin, which was identified by Alexander Fleming in 1928

70
Q

How was penicillin found?

A

The discovery of penicillin was a fortuitous accident, resulting from the unintended contamination of a dish containing S. aureus

A Penicillium mould began to grow on the plate and a halo of inhibited bacterial growth was observed around the mould

71
Q

What did Fleming conclude?

A

Fleming concluded that the mould was releasing a substance (penicillin) that was killing the nearby bacteria

72
Q

Who demonstrated the medical application of penicillin?

A

The medical applications of penicillin as an antibiotic were demonstrated by an Australian scientist, Sir Howard Florey, in 1940

73
Q

What did Florey and Chain test penicillin on?

A

Working with another scientist (Ernst Chain) and a team of researchers, Florey tested penicillin on infected mice

74
Q

What were the mouse infected with? Florey and Chain

A

Eight mice were injected with hemolytic streptococci and four of these mice were subsequently injected with doses of penicillin

75
Q

What were the results of Florey and Chain?

A

The untreated mice died of bacterial infection while those treated with penicillin all survived – demonstrating its antibiotic potential

76
Q

WHat is the historical significance of penicillin?

A

In 1945, Howard Florey, Ernst Chain and Alexander Fleming were collectively awarded the Nobel Prize for Medicine

Following the chemical determination of penicillin structure in 1945, several synthetic derivatives have since been created
These derivatives (including methicillin) offer many benefits including a broader spectrum, more stability and greater tolerance

77
Q

What is HIV?

A

The Human Immunodeficiency Virus (HIV) is a retrovirus that infects helper T cells, disabling the body’s adaptive immune system

78
Q

What is HIV collectively classified as?

A

It causes a variety of symptoms and infections collectively classed as Acquired Immuno-Deficiency Syndrome (AIDS)

79
Q

What does HIV target?

A

HIV specifically targets the helper T lymphocytes which regulate the adaptive immune system

80
Q

After infection, what does the HIV virus undergo?

A

Following infection, the virus undergoes a period of inactivity (clinical latency) during which infected helper T cells reproduce

81
Q

After a period of latency, what does the HIV virus do?

A

Eventually, the virus becomes active again and begins to spread, destroying the T lymphocytes in the process (lysogenic cycle)

82
Q

HIV - what does a reduction in number of helper T cells cause?

A

lymphocytes in the process (lysogenic cycle)
With a reduction in the number of helper T cells, antibodies are unable to be produced, resulting in a lowered immunity

83
Q

What does HIV result in, finally?

A

The body becomes susceptible to opportunistic infections, eventually resulting in death if the condition is not managed

84
Q

How is HIV transmitted, generally?

A

HIV is transmitted through the exchange of body fluids (including unprotected sex, blood transfusions, breastfeeding, etc.)

85
Q

How can the risk of HIV through sexual contact be reduced?

A

The risk of exposure to HIV through sexual contact can be minimised by using latex protection (i.e. condoms)

86
Q

Can you be immune to HIV infection?

A

YES
A small minority of people are immune to HIV infection (they lack the CD4+ receptor on TH cells that HIV requires for docking)

87
Q

Where is HIV particularly prevalent?

A

HIV is a global issue, but is particularly prevalent in poorer nations with poor education and health systems

Biology IB HL (56 decks)

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