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CNM Immune System > CNM Biomedicine S2 > Flashcards

CNM Biomedicine S2 Flashcards

1
Q

Describe the key differences between ‘innate immunity’
and
‘specific/adaptive immunity’

A

Innate immunity provides broad, non-specific immune response to any foreign substances and/or pathogens.

includes - physical barrier skin and mucous membranes and some immune cells, proteins and processes such as fever and inflammation.

In specific immunity a response is produced against a specific pathogen only

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2
Q

List four ways in which pathogens can enter the body

A

Through
- a break in the skin
- respiratory system
- digestive system
- reproductive system
- eyes

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3
Q

Define the following terms:

a. Antigens

b. Antibodies

A

a. An antigen is a substance (usually a protein molecule) that can be recognised by leukocytes and helps them to discern whether a cell is own or foreign

b. Antibodies are proteins that are produced in response to a specific antigen and combines with it

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4
Q

List five components of the first line of immune defence

A

Skin,
sweat,
sebum,
mucous,
mucociliary escalator, macroscopic nasal hairs,
saliva,
tears,
gastric acid,
vomiting,
diarrhoea

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5
Q

Explain what is meant by a
‘self-antigen’.

A

An antigen present on the cell membranes of the body’s own cells which identifies it to leukocytes.

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6
Q

How does the muco-ciliary escalator contribute to immune defence?

A

The cilia in the mucus membranes of the respiratory tract propels foreign particles towards the pharynx where they can be swallowed or coughed up.

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7
Q

How do the following contribute to immune defence:

a. Microflora
b. Gastric acid
c. Vagina

A

a. Microflora generally outcompete pathogens for attachment sites on epithelial cell surfaces
b. The acidity of gastric acid destroys many bacteria.
c. The vagina is acidic, making it unfavourable for microbes to inhabit.

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8
Q

Describe the role of transferrins

A

iron-binding proteins in blood which act to inhibit the growth of certain bacteria, by reducing the amount of available iron
(which bacteria could use for their growth).

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9
Q

List three ways in which the complement system destroys microbes

A

By promoting phagocytosis: the fragment C3b ‘coats’ microbes in a process called ‘opsonisation’ which promotes the attachment of a phagocyte to the microbe.
Contributes to inflammation: C3a and C5a bind to mast cells and cause them to release histamine.
Causes cytolysis by destroying microbes
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10
Q

Describe the role of the following cytokines:

Interleukin-1
Tumour Necrosis Factor (TNF)

A

Interleukins act as mediators between leukocytes. Interleukin-1 induces fever.
is produced by macrophages.
TNF promotes the accumulation of neutrophils and macrophages and causes cell death.

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11
Q

Describe the working of interferons in viral replication

A

Interferons are proteins that are produced by virus-infected cells. They diffuse to uninfected neighbouring cells and interfere with the viral replication process within these cells, halting the spread.

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12
Q

Name two phagocytic cells

A

Neutrophils

Macrophages

–

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13
Q

Explain the difference between ‘fixed’ and ‘wandering’ macrophages?

A

Wandering macrophages are monocytes that migrates to sites of infection and enlarge.
Fixed macrophages stand guard in specific tissues and do not move.

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14
Q

Name three locations of fixed macrophages

A

Kupffer cells in the liver
Alveolar macrophages in the lungs
Langerhans cells in the skin
Histiocytes in connective tissue
Microglia in nervous tissue
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15
Q

Describe in detail the five stages of phagocytosis

A

Chemotaxis: Chemicals released by microbes, leukocytes, damaged tissue and activated complement system attracts phagocytes.
Adherence: Attachment of phagocytes to the target (aided by complement)
Ingestion:
The cell membrane extends projections to engulf the microbe.
Digestion:
The ingested structure merges with lysosomes to form phagolysosomes and lysozymes digest it.
Excretion:
Indigestible material is excreted.
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16
Q

Describe specifically how Natural Killer cells cause cytolysis.

A

Natural Killer cells are lymphocytes that present in the blood, lymph nodes, spleen and bone marrow that attack anything they do not recognise. They bind to their target cell, release granules containing the protein ‘perforin’ which inserts into that cell’s membrane and creates a channel for tissue fluid to flow into the cell, causing it to burst.

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17
Q

List two factors that can trigger inflammation

A

Pathogens
Physical trauma (abrasions, wounds, breaks)
Chemicals
Extreme temperatures
Cell distortion or disturbance
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18
Q

Name five cardinal signs of inflammation

A

Heat
Redness
Swelling
Pain
Loss of function
–

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19
Q

List two benefits of inflammation

A

Inflammation promotes phagocytosis (increase in temperature promotes chemotaxis etc.)
Promotes immune response: vasodilation, increased permeability allows cells and proteins to leave the blood and enter the affected site.
Dilutes toxins
Fibrin formation: affected area is isolated
–

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20
Q

List two harmful effects of inflammation

A

Swelling: can be dangerous if in the cranium
Pain: can become chronic
Adhesions and scar tissue
Atherosclerosis: Inflammation is a key feature

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21
Q

Describe in detail the three stages of inflammation

A

Vasodilation and increased permeability: Allows additional blood, oxygen, nutrients, immune cells and repair substances to the area. More removal of toxins and dead cells. Redness, swelling and heat results and pain is due to injury to neurons and toxins released by microbes.
Emigration of phagocytes: Chemotaxis causes phagocytes to migrate to the scene
Tissue repair

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22
Q

Discuss the function and release site of the following inflammatory mediators:

Histamine
Leukotrienes
Kinins
Prostaglandins

A

Histamine is released by mast cells and basophils and causes vasodilation and increased permeability.
Leukotrienes are released by mast cells and basophils and they attract phagocytes and increase vessel permeability.
Kinins are peptides that are released in the blood which induce vasodilation and increased permeability. They attract phagocytes and interact with prostaglandins to induce pain.
Prostaglandins: Lipids released by damaged cells which enhance the effects of histamine and kinins.
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23
Q

List two functions of non-specific fever

A

Makes interferons more effective
Inhibits the growth of some microbes
Speeds up the reactions that aid repair
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24
Q

Name the cytokine that induces fever

A

Interleukin-1

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25
Q

In what autoimmune condition might a patient suffer from exophthalmos?

A

Grave’s disease

26
Q

List TWO signs / symptoms of AS

A

Sacroiliac and low lumbar spine pain
Worsening morning stiffness, improving with activity
Flattened lumbar lordosis leading to kyphosis

27
Q

Name two key functions shared by T- and B-lymphocytes

A

Both T- and B-lymphocytes:

possess specificity for antigens
produce immune memory for previously encountered antigens
usually recognises self-antigens from non-self antigens
–

28
Q

Describe the specific role of:

a. MHC-I
b. MHC-II

A

a. MHC-I are cell-surface proteins located on all body cells (except erythrocytes) allowing healthy body cells to be determined from abnormal/infected cells.
b. MHC-II are located only on the cell membrane of ‘antigen presenting cells’ (macrophages & B-lymphocytes) for displaying foreign antigens to T-helper cells.

29
Q

Describe the role of cytokines between the innate and adaptive immune systems.

A

Cytokines are small protein hormones secreted by leukocytes and are basically messenger molecules that mediate the connection between the innate and adaptive immune system.

30
Q

Discuss the following statement:

‘T- and B-lymphocytes are normally activated’

A

T- and B-lymphocytes function in adaptive immunity, whereby they learn to respond to foreign antigens. They are only activated each for a specific antigen.

31
Q

Name the body cell that does not contain MHC-I

A

Erythrocytes

32
Q

Explain the role of TCR (T-cell receptors)

A

T-cells play a central role in cell-mediated immunity. Millions of different T-lymphocytes exist, each with a unique T-cell receptor (TCR) that only recognises a specific antigen.

33
Q

Name the following T-cells:

a. CD4
b. CD8

A

a. T-helper cells

b. Cytotoxic T-cells

–

34
Q

Describe the difference between ‘self-recognition’ and ‘self-tolerance’

A

Self-recognition is the ability to recognise self-antigens and ‘self-tolerance’ is the lack of reactivity to fragments of self-antigens.

35
Q

List TWO differences between ‘cell-mediated immunity’ and antibody-mediated immunity’

A

Cell-mediated immunity is through T-lymphocytes where cytotoxic T-cells directly attack invading agents and defends against mostly intra-cellular pathogens.
Antibody-mediated immunity is by B-lymphocytes that transforms into plasma cells which synthesise and secrete specific antibodies to defend mostly against extra-cellular pathogens.

–

36
Q

Describe in detail how an antigen is presented to a T-helper cell leading to and including clonal selection

A

Antigen-presenting cells (macrophages and B-cells) come accross foreign antigens and ingest and combine them with MHC-II complexes on their cell membrane. They then migrate into lymphatic tissue where they ‘present’ the antigen to T-helper cells (CD4). When these antigen fragments bind with the T-helper cell, it secretes a cytokine, interleukin-2 which cause the T-helper cell to undergo clonal selection. Clonal selection produces Cytotoxic T-cells, Memory T-cells and Helper T-cells.

37
Q

Describe the key functions of the following T cells:

a. Cytotoxic T-cells
b. Memory T-cells
c. Helper T-cells
d. Regulatory T-cells

A

a. Cytotoxic T-cells: binds to target cell and destroy it using protein digesting enzymes - granzymes & perforin
b. Memory T-cells: They are inactive but recognise the antigen with any future contact, ready to mount an immune reaction
c. Helper T-cells: release cytokines which increase the activity of immune cells such as B-, T- and NK cells
d. Regulatory T-cells: a specialised sub-population of T-cells which deactivate immune cells when an immune response is no longer required, thereby helping to maintain immune system homeostasis and tolerance to self-antigens.

–

38
Q

Name TWO outputs of B-cell clonal selection

A

Plasma cells

Memory B-cells

39
Q

Name the cytokine that triggers clonal selection

A

Interleukin-2

40
Q

Describe how antibodies combine with antigens

A

Antibodies generally have two antigen binding sites and they bind specifically with the antigen that stimulated their prodution in a ‘lock and key’ fashion.

41
Q

Describe the role of:

a. Plasma cells
b. Memory B-cells

A

a. They secrete antibodies into the blood, producing only one type of antibody. Secretes hundreds of millions of short-lived antibodies a few days after exposure.
b. They are long-lived and remember antigen for next time, ready to produce more plasma cells for a second immune reaction

42
Q

Describe the role of:

a. Plasma cells
b. Memory B-cells

A

a. They secrete antibodies into the blood, producing only one type of antibody. Secretes hundreds of millions of short-lived antibodies a few days after exposure.
b. They are long-lived and remember antigen for next time, ready to produce more plasma cells for a second immune reaction

43
Q

Interleukin-2

–

Describe how antibodies combine with antigens

A

Antibodies generally have two antigen binding sites and they bind specifically with the antigen that stimulated their prodution in a ‘lock and key’ fashion.

44
Q

Describe in detail THREE ways antibodies can inactivate an antigen

A

Neutralise: bacterial toxins or prevent viral attachment to cells
Immobilise: antigens by binding to bacterial cilia or flagellae
Agglutinate and precipitate: use both their binding sites to cause clumping of cells
Activating compliment: Antigen-antibody complexes activate the complement cascade
Enhances phagocytosis: The antibody acts as a flag to attract phagocytes and aids phagocytosis via agglutination and complement
–

45
Q

Name the most abundant antibody in the body

–

A

IgG

46
Q

Briefly describe how immunological memory develops.

A

Immunological memory is based on the presence of long-lasting antibodies and very long-lasting memory B- and memory T-cells.
The primary response is slow and antibodies do not appear for several days, then a slow rise in IgM, followed by IgG.
The secondary response is much faster and can be decades later since memory cells last very long. It is often so effective, the microbe is killed off before any signs or symptoms

47
Q

Explain the difference between:

a. Naturally acquired and artificially acquired active immunity
b. Naturally acquired and artificially acquired passive immunity

A

a. Naturally acquired active immunity is in response to the natural exposure to a disease. Artificially acquired active immunity is via vaccination.
b. Naturally acquired passive immunity is via the transfer of IgG antibodies accross the placenta from mother to child and IgA antibodies via breastmilk. Artificially acquired passive immunity is via the injection of immunoglobulins as in the case of snake anti-venom.

48
Q

Describe the pathophysiology of the following hypersensitivity reactions:

Type I
Type II
Type III
Type IV

A

Type I Hypersensititvity is known as an allergy. It is mediated by IgE antibodies that bind to mast cells, causing degranulation. Reactions can be systemic eg. anaphylaxis, or localised eg. hay fever, eczema. The onset is rapid.
Type II Hypersensitivity is seen in haemolytic disease of the newborn / blood transfusion reactions. IgG antibodies are produced by the immune response and the antigen antibody complexes activate the complement system. The onset is rapid.
Type III Hypersensitivity is seen in glomerulonephritis, rheumatoid arthritis and systemic lupus erythematosus. Antibody-antigen complexes form and are deposited in capillaries, skin, joints and kidney, triggering an immune response. Complement system is activated. IgM, IgG and IgA mediated. Onset in 4-8 hours
Type IV Hypersensitivity is cell-mediated and associated with an over-reaction of T-lymphocytes to an antigen. Large numbers of cytotoxic T-cells are activated and cytokines are released, possibly damaging normal tissue. It is seen in MS and dermatitis and onset is delayed: 48 - 72 hours
–

49
Q

List one pathology for each of the following hypersensitivity reactions:
Type I
Type II
Type III
Type IV

A

Type I: Eczema; Allergies
Type II: Haemolytic disease of the newborn
Type III: Rheumatoid arthritis; SLE
Type IV: MS; dermatitis

50
Q

Name TWO immunoglobulins that mediate a Type III hypersensitivity reaction.

A

IgM, IgG, IgA

51
Q

List FOUR common allergens

A

Dust
Pollen
Mites
Latex
Certain foods (peanuts, milk, wheat)
Animal dander
Chemicals / perfumes / detergents / soaps
–

52
Q

Describe the pathophysiology of an ‘allergy’

A

The initial exposure to an allergen causes sensitisation but this is a slow response. The body then produces IgE specifically for that allergen (B-Cell > plasma cell > specific antibody).
Subsequent exposure triggers an exaggerated immune response for which the antibodies are readily available. IgE cross-links mast cells and the allergen. Symptoms can range from a mild runny nose to fatal anaphylaxis.

53
Q

Explain the key difference between a ‘food intolerance’ and a ‘food allergy’

A

Food allergies affect 2% of adults, 6% of children and are IgE mediated and can be triggered by even the smallest amount of food.
Food intolerances do not have a defined immune response, but symptoms are triggered by ingesting a quantity of a specific food when digestive factors are lacking to deal with it, such as enzymes, bile, HCl or probiotics.

54
Q

Define ‘auto-immunity’

A

Autoimmune disorders are conditions associated with an immune response against the body’s own tissues due to a breakdown of mechanisms responsible for self-tolerance.

–

55
Q

Describe the pathophysiology of the following:

a. Systemic lupus erythematous (SLE)
b. Rheumatoid arthritis (RA)
c. Ankylosing spondylitis (AS)

A

a. In SLE, anti-nuclear antibodies are formed. This occurs through B-cell activation which increases IgG levels against components of cell nuclei. There is impaired immune regulatory mechanisms: immune complexes are not removed from tissues and complement is activated, causing inflammation. There is impaired T-cell regulation.
b. In RA, there is chronic inflammation of many tissues, primarily the synovium. It occurs when Rheumatoid Factor, an auto-antibody binds to IgG to form an immune complex which activates complement and leads to inflammation.
c. Ankylosing spondylitis is a systemic autoimmune disease with chronic inflammation of the spine and sacroiliac joints, often leading to spinal fusion and stiffness. There is a strong genetic association with HLA-B27 and links with inflammatory bowel diseases, leaky gut and infections such as salmonella and shigella cross-reacting with HLA-B27.

56
Q

Name TWO causes of SLE

A

High oestrogen levels
Low vitamin D levels
Chronic bacterial infections / viral infections eg. EBV
Smoking, silica dust

57
Q

List TWO triggers of SLE

A

Stress
UV light
HRT / oral contraceptive pill
pesticides

58
Q

State TWO characteristic signs / symptoms of SLE

A

Butterfly rash on face
Joint aches and pains
Photosensitivity
Raynaud’s syndrome
Pleurisy
–

59
Q

Name ONE unique blood test used to identify SLE

A

ANA (Anti-nuclear antibodies)

60
Q

List ONE gene associated with:

a. Rheumatoid arthritis (RA)
b. Ankylosing spondylitis (AS)

A

a. HLA-DR4 / DR1

b. HLA-B27

61
Q

Name THREE signs / symptoms of RA

A

Bilateral arthritis of small joints
Progressive morning stiffness > 1 hour
Deformity of joints eg. swan neck, ulnar deviation
Subcutaneous nodules

62
Q

List TWO bacterial causes/triggers of AS

A

Salmonella

Shigella

CNM Immune System (2 decks)

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