Immune System Flashcards

1
Q

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

A

Innate immunity is inborn or natural and it is non specific. It attacks anything that our body perceives as foreign or dangerous.

Specific/adaptive immunity is activated by the innate immune system producing a response to a specific pathogen. It creates immune cells with memory against specific foreign cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List FOUR ways in which pathogens can enter the body.

A

Break in the skin
Respiratory System
Digestive System
Male/female reproductive systems
Eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define the following terms:

a. Antigens

b. Antibodies

A

a. Antigens

A substance (usually proteins) that can be recognised by leukocytes. It acts like a marker or flag or passport.

b. Antibodies

Proteins that are produced in response to a specific antigen. They combine with these specific antigens.

When antigens and antibodies join together they create an immune response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Any cell that is one of our own will contain lots of self antigens on the cell membrane. They say I’m safe, I’m part of you and here is the proof.

Foreign antigens are antigens that we have not produced ourselves. We find them on cells like bacteria or viruses. When a leukocyte stroll by and sees its passport it will want to get rid of it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe how the following contribute to the first line of immune defence:

a. Sweat

b. Sebum

c. Saliva

d. Tears

A

a. Sweat;
* Sweat glands on the dermis contain antibodies called IgA
(Ig = immunoglobulin = antibody)
A = first letter of the alphabet and first layer of our body = saliva, sweat, tears, mucus secretions all have IgA

  • sweat secreted onto the skin surface, contains antibacterial and antifungal substances which remove microbes from the skin

b. Sebum
* Contains fatty acids which inhibit microbial growth

c. Saliva
* Wash away food debris they may have microbes
* contain anti-microbial substances
* Contain IgA and lysozymes. Lysozymes are enzymes that break down bacterial cell walls.

d. Tears
o Wash away microbes on the surface of the eyes, and also contain anti-microbial substances.
o Contain IgA and lysozymes. Lysozymes are enzymes that break down bacterial cell walls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain how the mucociliary escalator contributes to immune defence.

A

Cilia propel the foreign substances toward the pharynx where they are swallowed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe how the following contribute to immune defence:

a. Microflora

b. Gastric acid

c. Vagina

d. Urine/faeces

e. Vomiting/diarrhoea

A

a. Microflora
Generally out compete pathogens for (i) the attachment sites on the epithelial cell surfaces (ii) essential nutrients

b. Gastric acid
The acidity destroys many bacteria. Very acidic at 2-3 PH.

c. Vagina
Acidic environment in menstruating women making it unfavourable for microbes to inhabit

d. Urine/faeces
Expels microbes

e. Vomiting/diarrhoea
Rapid means of expelling pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the role of transferrin’s.

A

2nd line of defence. Iron binding proteins in the blood. They latch on to iron, binding to it, shielding it and stopping bacteria from using it. Bacteria love iron and use it for growth.

Transferrins are in the blood because that is where we find iron.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List THREE ways by which the complement system destroys microbes.

A
  1. Promoting Phagocytosis:

The activated C3b fragment attaches to microbes in a process called opsonisation.

It acts as a kind of tracking device alerting incoming neutrophils and macrophages that this is the cell that needs to be attacked.

  1. Contributing to inflammation
    C3a and C5a bind to receptors on mast cells and cause them to release histamine.
  2. Causing Cytolysis
    A hole is created in the microbe allowing fluid in causing the cell to swell, distend and then rupture.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a cytokine?

A

Cytokines are small protein hormones that stimulate or inhibit normal cell functions.

They are secreted by Leukocytes.

They act on cells involved with immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the role of the following cytokines:

a. Interleukin-1

b. Tumour necrosis factor

A

a. Interleukin-1

Interleukins are a group of cytokines that act as mediators between leukocytes. They are really important in the immune response. Names Interleukin 1,2, 3, 4 etc.

Interleukin 1 is released by macrophages when engulfing a pathogen. It goes into the blood and travels to the brain where it tells the hypothalamus to increase body temperature. This leads to a fever.

So interleukin 1 is the messenger between the macrophage and the hypothalamus saying please increase temp.

b. Tumour necrosis factor
Protein that attracts neutrophils and macrophages to the area and can cause cell death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Discuss the following statement:

‘Interferons stop viral replication’

A

Interferons are a type of cytokine (along with Interleukins and Tumour Necrosis Factor).

Interferons are antiviral proteins produced by cells that are infected by a virus. Interferons ‘interfere’ by telling all of the cells surrounding the virus to stop dividing.

The way that viruses grow is through replication inside our host cells. However they can only do this once they are inside the cell where they can integrate their own DNA and then get our cells producing their own DNA.

Therefore one of our strategies needs to be stopping the surrounding cells from dividing and thus replicating the virus.

Eg: someone comes to the door that no one wants to see. Interferons send a Whatsapp message to everyone else saying X is at the door. Keep the door shut and stay quiet until they leave.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name TWO phagocytic cells.

A

The two major types of phagocytic cells are macrophages and B lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are Macrophages?

A

Antigen presenting immune cells.

Known as Monocytes in white blood cells and macrophage when they migrate from the bloodstream into any tissue in the body.

Macrophages break down the pathogen using lysozymes. Most of what is broken down is excreted but some of it will be displayed on the cell membrane of its own structure. This ‘foreign antigen’ is presented to T-Lymphocytes so that they learn about the threats in the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

Wandering Macrophages are formed from monocytes that migrate to the site of infection and enlarge.

Fixed macrophages are fixed and stand guard in specific tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name THREE locations for fixed macrophages.

A
  1. Histiocytes (connective tissue macrophages).
  2. Kupffer cells (only in the liver).
  3. Alveolar macrophages (lungs).
  4. Microglia (nervous tissue).
  5. Langerhans cells (skin).
  6. Tissue macrophages (spleen, bone marrow, lymph nodes).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe in detail the FIVE stages of phagocytosis.

Hint : CAIDE

A

1. Chemotaxis (to attract phagocytes)
The release of chemicals by
- microbes
- leukocytes
- damaged tissue and,
- activated complement

(As soon as you damage an area of tissue or have microbes in an area or have proteins being released by leukocytes, there will be lots of triggers than attract phagocytes to the area.)

2. Adherence
Attachment of the phagocyte to the target. Phagocytes have these extensions that attach onto the foreign cell. When they attach that is known as adherence.

(Granuloma: Some microbes are resistant to adherence. TB is an example and this means that TB is resistant to the whole phagocytosis process so we have to do something different. Instead, we surround it with layers of immune cells.)

3. Ingestion
The cell membrane extends projections that engulf the microbe.

4. Digestion
The engulfed microbe merges with lysosomes that have digestive enzymes called Lysozymes which digest the microbe.

5. Excretion
Whatever is not ingested in the stage 4 is excreted. The indigestible material.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

List five components of the first line of immune defence

A
  • Skin
  • Mucus membranes
  • Mucociliary escalator
  • Vomiting
  • Diarrhoea
  • Saliva
  • Tears
  • Sweat
  • Sebum
  • Nasal hairs
    *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where are the complement proteins produced? Explain the role of the complement.

A

Produced in the liver
Produce a cascade of immune response that leads to
- inflammation
- phagocytisis and
- cytolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe specifically how natural killer cells cause cytolysis.

A

Through cytolosis which is one of the three ways by which the complement system destroys microbes.

  • NK cells bind to a target cell and release granules containing the protein perforin
  • Perforin can be likened to a spear that perforates the foreign organism cell membrane creating a hole for tissue fluid to flow into the cell and causing it to rupture.
  • Being non-specific they attack anything with a foreign antigen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

List TWO factors that trigger inflammation.

A
  1. Pathogens
  2. Abrasions
  3. Chemicals
  4. Damage to a tissue
  5. Extreme temperatures.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name THREE cardinal signs of inflammation.

A
  1. Redness
  2. Heat
  3. Pain
  4. Swelling
  5. Loss of Function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

List TWO harmful effects of inflammation.

A
  • Swelling can be dangerous, for example in the cranium leading to ICP
  • Pain can become chronic
  • Scar tissue and adhesions if continuous inflammation. Eg: endometriosis
  • Atherosclerosis inflammation is a key feature of this process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the THREE stages of inflammation.

A

Stage 1: Vasodilation and increased permeability.
Stage 2: Emigration of phagocytes
Stage 3: Tissue Repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What happens in the THREE stages of inflammation?

A

Stage 1: Vasodilation and increased permeability.

Increased blood flow from vasodilation
- brings oxygen, nutrients, immune cells and repair substances
- Removes toxins and dead cells.

Increased permeability permits the movement of
- immune cells
- defence cells such as antibodies, and
- clotting factors into the tissue.

Stage 2: Emigration of phagocytes
Within an hour of the process beginning, phagocytes migrate to the scene (via chemotaxis).
* Neutrophils stick to the endothelium during vasodilation and squeeze through the vessel wall to reach the damaged area (leukocytosis).
* Monocytes quickly follow and transform into wandering macrophages.
* Dead phagocytes accumulate as pus

Stage 3: Tissue Repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

With regards to following inflammatory mediators, what are they released by and what is their function?

Histamine:

Leukotrienes:

Kinins:

Prostaglandins:

A

Histamine
Released by: Mast Cells and Basophils
Function:
- Increased permeability
- Vasodilation

Leukotrienes
Released by: Mast Cells and Basophils
Function:
- Increased permeability
- Attract Phagocytes

Mediator: Kinins
Released by? ???
Function:
- Increase permeability
- Induce vasodilation
- Attract phagocytes
- Induce pain

Mediator: Prostaglandins
Released by: Damaged Cells
Function:
- Locally-acting vasodilators
- prevent needless clot formation
- inflammation
- Ehance effects of histamine and kinins (and so intensify pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

List TWO functions of non-specific fever.

A

a. Makes interferons more effective.
b. Inhibits growth of some microbes.
c. Speeds up the reactions that aid repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Name the cytokine that induces fever.

A

Interleukin-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

List TWO key functions shared by T- and B-lymphocytes.

A

T and B Lymphocytes are both produced in bone marrow but mature in different places – the thymus and the red bone marrow respectively.

Key functions:
- Possess specificity for particular antigens meaning that they specialise in one particular antigen. When that antigen is not evident they are at rest.
- Produce immune memory for previously encountered antigens which allows them to recognise them quickly and act quickly next time they encounter them.

30
Q

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

A

Cytokines are messenger molecules that mediate the connection between the innate immune system and the adaptive immune system

31
Q

When are T-lymphocytes and B-lymphocytes normally activated?

A

T- and B-lymphocytes are normally at rest.

They become activated on encountering a foreign antigen (or what they perceive to be foreign).

T-lymphocytes are activated when they encounter antigens presented by antigen-presenting cells.

B-lymphocytes are activated when their surface antibodies bind to specific antigens

32
Q

Describe the specific role of:

a. MHC-I

b. MHC-II

A

MHCs are a group of cell-surface proteins that are required for the immune system to recognise cells that are healthy body cells versus those that are ‘non-self’.

a. MHC-I

Every single sell in the body (except erythrocytes) will have MHC-1.
Its job is to combine with proteins produced by the cell to display proteins on on the cleft shaped binding groove of the MHC-1 of the cell membrane.
If the cell has been damaged or invaded by a pathogen the proteins produced will be abnormal and leukocytes will bind to it and initiate a series of immune responses to destroy the compromised cell.

b. MHC-II

The only cells that have MHC-II will be the antigen presenting cells such as Macrophages and B – Lymphocytes.

It is used to display whatever they have broken down. If that macrophage digests a foreign cell it displays the foreign antigen on the cleft shaped binding groove of MHC-II so that it can present it to T-Helper cells which initiate a set of defensive responses.

33
Q

Name the body cell that does not contain MHC-I.

A

Erythrocytes

34
Q

Explain the role of TCR (T-cell receptors).

A

The T-cell receptor ( TCR) is a protein complex found on the surface of T cells, or T lymphocytes.

Millions of different T-lymphocytes exist, each with a unique T-cell receptor (TCR) that only recognises a specific antigen

35
Q

Name the following T-cells:

a. CD4

b. CD8

A

a. CD4 – T-Helper and Macrophages

b. CD8 – Cytotoxic T-Cells

36
Q

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

A

Self recognition is the ability to recognise self antigens

Self tolerance is the need to not react to fragments of self antigens

37
Q

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

A

They are both types of adaptive immunity which is characterised by specificity for a particular foreign antigen and the production of immune memory.

Cell mediated immunity involves T lymphocytes
- defends mostly against intracellular pathogens, so pathogens within the cell
- Cytotoxic T cells directly attack invading antigens

Antibody mediated immunity involves B lymphocytes
- defends mostly against extra cellular pathogens
- B cells transform into plasma cells, which synthesise and secrete specific antibodies (Igs)

38
Q

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

Clue - 4 steps

A

Step 1:
Macrophages and B-Cells combine a fragment of broken down foreign antigen with MHC-II and present it on their membrane.

Step 2:
Antigen presenting cells migrate intolymphatic tissue and present antigen to T-Helper cells.

Step 3:
The antigen fragment combines with the the T-helper which triggers the T Helper cell to secrete the cytokine interleukin-2

Step 4 - IL-2 causes the T Helper cells to undergo clonal selection.

Step 4:
Activation and proliferation of T-cells
* Clonal selection of B-cells

39
Q

Name the cytokine that triggers clonal selection.

A

Clonal selection refers to the division and proliferation of activated T-cells

Interleukin-2 is the cytokine that stimulates this process.

40
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

These are all cells involved in clonal selection where we get the division and proliferation of T-Cells

a. Cytotoxic T-cells
Main type of T lymphocyte that actively go out and try to break down and destroy foreign cells.

b. Memory T-cells
Emerge when we’ve had an active exposure producing immune memory for an antigen oncve it has been encountered.

c. Helper T-cells
Mediates the immune response – don’t do the killing, do the admin for the entire 3rd line of defence for both T and B cells

d. Regulatory T-cells
turn off an immune reaction when the immune response should be finished.

41
Q

Name TWO outputs of B-cell clonal selection.

A

Plasma Cells
Memory B-Cells

42
Q

B-Cell clonal selection produces two types of cells. Describe their role:

A

a. Plasma cells – Throw out lots of one type of antibody.

Few days after antigen exposure, plasma cells secrete hundreds of millions of antibodies into the blood each day until cells die

Short-lived

b. Memory B-cells - remain inactive in case of a subsequent infection.

Remember antigen for next time, ready to proliferate and produce more plasma cells for a second immune reaction

Long-lived.

43
Q

Draw and label an ‘antibody

A

Y shaped structure that has 4 polypeptide chains, two binding sites, a contant region and a variable region.

44
Q

Describe how antibodies combine with antigens.

A
  • Antibodies generally have two antigen-binding sites.
  • Antibodies combine specifically with the antigen that triggered their production- its called lock and key because only they fit each other.
  • They form antibody-antigen immune complexes.
45
Q

Describe in detail THREE ways antibodies can inactivate an antigen.

(5 potential Answers)

A
  1. Neutralising: - If bacterial toxins are present we can use antibodies to bind to those bacterial toxins and subsequently inactivate those toxins and prevent their harmful effects.
  2. Immobilising: Bind to antigens on bacterial cilia or flagellae. Essentially catch them so they can’t get away
  3. Agglutinating and precipitating: Antibodies use both their two binding sites to cause clumping of cells.
  4. Activating complement: Antigen-antibody complexes activate the complement cascade – attracting phagocytes and causing inflammation
  5. Enhancing phagocytosis: The antibody acts as a flag to attract phagocytes and aids phagocytosis via agglutination and complement.
46
Q

Name the most abundant antibody in the body.

A

IgG – 80% of antibodies

47
Q

Briefly describe how immunological memory develops.

A

Stage 1: Primary Response
This is the slow response on first exposure where antibodies start to appear after a few days and then we see a slow rise in IgM followed by IgG

Stage 2:Secondary Response for any subsequent exposure
* This is a much faster response because a full immune response has been developed with thousands of memory cells
* Often the secondary response is so effective, it kills off the microbe before you exhibit any signs or symptoms.
* Memory cells can last decades.

Immunological memory is the basis for vaccination against certain diseases.

48
Q

Explain the difference between:

a. Naturally acquired and artificially acquired active immunity

b. Naturally acquired and artificially acquired passive immunity

A

Active is where the body has a role in creating the immunity

Passive is when the body does not need to do anything because the immunity is given to it.

a. Naturally acquired and artificially acquired active immunity

Naturally aquired AND active - we have a natural exposure to a disease like sitting next to someone that is coughing and you catch the cough.

Artificially acquired AND actively, we have exposure to a disease but through intervention such as vaccination

b. Naturally acquired and artificially acquired passive immunity

Naturally AND passively the immunity is formed by being passed on to you:
- Transfer if IgG antibodies across the placenta
- Transfer if IgA antibodies from breast milk

Artificially AND passively it is an injection of antibodies (immunoglobulins) for something like a snake bite where the body does not need to do anything

49
Q
  1. Describe the pathophysiology of the following hypersensitivity reactions:

a. Type I

b. Type II

c. Type III

d. Type IV

A

Hypersensitivityrefers to an excessive immune response produced by a normal immune system.

Type 1, 2, and 3 are all antibody mediated meaning that antibodies generate this immune response.

Type 4 is cell-mediated so cytotoxic cell mediated

a. Type I
* Allergy
* Mediated by IgE antibodies that bind to mast cells.
* Results in the release of inflammatory mediators (e.g., histamine, prostaglandins, leukotrienes, kinins, serotonin)
* Onset is rapid

b. Type II
* IgG antibodies produced by the immune response
* As seen in haemolytic disease of the newborn and blood transfusion reactions.
* Only IgG antibodies that can go through the placenta
* Onset is rapid

c. Type III
* Involves III antigens - IgG, IgM, IgA
* Autoimmune disorder - Glomerulonephritis; RA: SLE
* Antigen antibody complexes deposit in certain parts of the body and activate the complement system.
* Onset in four - eight hours.

d. Type IV
* Skin graft, MS
* There is an overreaction of T-Cells to an antigen.
* Large numbers of cytotoxic T-cells activated and cytokines released that can start to break down normal cells that are healthy.
* Delayed type hypersensitivity: 48 - 72 hours

50
Q

List one pathology for each of the following hypersensitivity reactions:

a. Type I

b. Type II

c. Type III

d. Type IV

A

a. Type I
Systemic – Anaphylaxis
Localised: Hayfever, eczema, irritant contact dermatitis

b. Type II
Haemolytic disease of the newborn

c. Type III
RA; Glomerulonephritis

d. Type IV
MS

51
Q

Name TWO immunoglobulins that mediate a Type III hypersensitivity reaction.

A

IgG, IgA, IgM

52
Q

List FOUR common allergens.

A

An allergen is an antigen that generates allergy. The allergen itself is usually harmless, it is the immune response that causes damage.

Pollen
Dust
Latex
Certain foods
Animal dander

53
Q

Describe the pathophysiology of an ‘allergy’.

A

An allergy is an exaggerated immune response to substances that are usually harmless to most people. The process can be broken down into several key steps:

  1. **Sensitisation: **
    Initial exposure causes sensitisation — a slow response as not many cells have the correct specificity to respond to the antigen (allergen) as they have not been activated.
  2. **Production of IgE antibodies **specific to the particular allergen encountered.
  3. Subsequent exposure: is an exaggerated immune response. The full immune response has been developed and antibodies are readily available.
  4. Release of inflammatory mediators: The binding of the allergen to IgE triggers the release of inflammatory mediators, such as histamine, from the mast cells and basophils.
    Histamine and other mediators cause various symptoms of an allergic reaction, including vasodilation, increased vascular permeability, and smooth muscle contraction
    5.Immediate hypersensitivity reaction: The release of inflammatory mediators leads to the classic symptoms of an allergic reaction, such as itching, redness, swelling, and increased mucus production
54
Q

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

A

A true food allergy is an IgE mediated immune response and only affects 2% of adults and 6% of children.

Food intolerance does not have a defined immune response. Symptoms are triggered by eating a quantity of a particular food and lacking enzymes, probiotics, bile, HCl, or other digestive factors needed to deal with the food.

55
Q

Define ‘auto-immunity.

A

A breakdown of mechanisms responsible for self-tolerance.

56
Q

Describe the pathophysiology of Systemic lupus erythematous (SLE)

A

A chronic inflammatory, autoimmune, multi-system disorder in which autoantibodies are formed against nuclear antigens meaning that we get antibodies formed against any cell in the body that has a nucleus.

It follows a relapsing-remitting course.

The exact cause of SLE is not fully understood, but it is believed to involve a combination of genetic, environmental, and hormonal factors. The pathophysiology of SLE is complex and involves immune dysregulation, inflammation, and tissue damage.

> > B-cell activation, increasing IgG levels against components of cell nuclei (DNA, nucleic acids etc)

> > Impaired immunity regulatory mechanisms lead to the inability to remove immune complexes from tissue. The immune complexes can deposit in various tissues, particularly in the kidneys, joints, skin and blood vessels leading to activation of complement and therefore inflammation.

Chronic inflammation and the deposition of immune complexes in various organs can lead to tissue damage and organ dysfunction.

Organs commonly affected in SLE include the skin, joints, kidneys, heart, lungs, blood vessels and the nervous system.

> > > Impaired T-Cell regulation dysregulates the switching off of the immune system

> > > The combination of these factors results in a dysregulated immune response, chronic inflammation, and the potential for severe organ damage in individuals with SLE.

57
Q

Describe the pathophysiology of Rheumatoid arthritis (RA)

A

Chronic, systemic inflammation of many tissues, primarily the synovium (potentially all organs except brain).

Antibodies (Rheumatoid Factor) are created and directed against other antibodies (IgG). So essentially RF is an antibody is attacking other antibodies in the blood. They create immune complexes that start depositing in areas like joints and other tissues.

The resultant immune complexes activate complement proteins leading to inflammation.

58
Q

Describe the pathophysiology of Ankylosing spondylitis (AS)

A

AS is a systemic autoimmune disease associated with chronic inflammation of the spine and sacroiliac joints, often leading to spinal fusion (ankylosis) and stiffness.

Typically begins at the very bottom of the spine – at the little dimples at the base of your back - where the sacroiliac joints are. These joints get inflamed from here and then ascend up the spine causing stiffness in the spine and lower back.

Over time patients become kyphotic as the vertebrae fuse together and we see bamboo spine

59
Q

Name TWO causes of SLE.

A

SLE is caused by a multifactorial interaction between various genetic and environmental factors.

  • Higher oestrogen levels have been linked to onset.
  • Links with low vitamin D levels.
60
Q

List TWO triggers of SLE.

A
  • Certain viral infections, such as Epstein-Barr virus, have been linked to the development or exacerbation of SLE in some cases. The immune response triggered by infections may contribute to the development of autoimmune diseases
  • Hormone effects through the contraceptive pill or HRT
  • Stress
  • Sunlight Exposure: Ultraviolet (UV) light from the sun can trigger skin rashes and worsen symptoms in individuals with SLE, especially those with photosensitivity
61
Q

State TWO characteristic signs / symptoms of SLE.

A
  • Butterfly rash
  • Photosensitivity
  • Vasculitis – pain in fingertips
  • Raynaud’s disease
  • Joint pain
62
Q

Name ONE unique blood test used to identify SLE.

A
  • Anti-nuclear antibodies is a unique test for SLE.
  • Anaemia, elevated ESR and complement are others but they are not unique
63
Q

List ONE gene associated with:

a. Rheumatoid arthritis (RA)

b. Ankylosing spondylitis (AS)

A

a. Rheumatoid arthritis (RA)
HLA – DR4
HLA – DR1

b. Ankylosing spondylitis (AS)
HLA - B27

64
Q

Name THREE signs / symptoms of RA.

A
  • Stiff for more than an hour in the morning
  • Symmetric pain in the smaller joints usually the hands and feet to start with
  • Deformity of joints
  • Subcutaneous nodules around fingers and elbows
  • Systemic signs are general fatigue and malaise
65
Q

List TWO bacterial causes/triggers of AS

Ankylosing spondylitis

A

It has links with urogenital or intestinal infections such as salmonella and shigella cross reacting with HLA-B27

66
Q

List TWO signs / symptoms of AS.

A
  • Lower back symptoms often improve with activity.
  • The lumbar lordosis flattens and patients often become kyphotic.
  • Hip and heel (Achilles) pain are common.
67
Q

What lymphocyte is implicated in antibody mediated immunity?

A

B-Lymphocyte

68
Q

Explain the role of interleukin 2

A

Interleukin-2 is a cytokine that is
- the prime trigger for T-lymphocyte proliferation and,
- stimulates clonal selection of B-lymphocytes where we create
* T-Helper cells, cytotoxic T-cells and memory T cells
* Plasma cells and memory B-cells

69
Q

Name two antigen presenting cells

A

Macrophages and B-cells

70
Q

Where does self recognition and self tolerance of T cells occur

A

In the thymus where they mature

71
Q

What autoimmune condition might have patients suffer from Exophthalmos

A

Axopthalmis is bulging eyes.

Graves disease which is an immune system disorder that results in the overproduction of thyroid hormones (hyperthyroidism).

72
Q

What are thought to be the causes of Ankylosing Spondylitis litis?

A

There is also a strong genetic association. 95% of AS patients have the HLA-B27 marker

Links with inflammatory bowel disease

Links with euro genital or intestinal infections, such as salmonella and Shigella cross reacting with HLA- B27