year 4 CMS > Immunology > Flashcards

Immunology Flashcards

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1
Q

What are the two main categories of immune defences?

A

Non-specific (innate) and specific (adaptive) immunity.

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2
Q

How old is the immune system in evolutionary terms?

A

Very old; even single-cell organisms demonstrate immunity. It evolved with use, explaining its complexity.

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3
Q

What are the key physical/mechanical barriers in innate immunity?

A

Skin, mucosa, respiratory cilia, and fluid flow.

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4
Q

Why is skin an effective immune barrier?

A

It is a semi-permeable membrane protecting organs; cells reproduce rapidly to withstand damage and invasion.

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5
Q

How does mucosa protect the body?

A

Thick, tough structures that withstand external invasion.

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6
Q

What is the function of respiratory cilia?

A

Beat in a coordinated fashion, sweeping trapped bacteria/viruses in one direction; most inhaled pathogens are trapped in mucosa.

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7
Q

How does fluid flow act as a defence?

A

Flushes pathogens away (e.g., urine flow preventing UTIs).

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8
Q

What can happen if fluid flow is reduced?

A

Ascending infections → cystitis, kidney infections, acute ascending parotitis (often when dehydrated/run-down).

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9
Q

What chemical secretions contribute to innate immunity?

A

Stomach acid and other digestive secretions.

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10
Q

How does stomach acid kill pathogens?

A

Denatures proteins, destroying bacteria and viruses.

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11
Q

What triggers inflammation?

A

Bacteria, viruses, fungi, tissue damage, chemicals released from dead cells.

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12
Q

What are the key steps of inflammation?

A

Vasodilation → more blood flow Increased vascular permeability → WBCs enter tissues Chemotaxis → WBCs move down cytokine/bacterial gradients Phagocytosis → digest pathogens/dead cells Formation of exudate and oedema

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13
Q

What do WBCs do during inflammation?

A

Are phagocytic Kill pathogens via enzymes/chemicals Act as antigen-presenting cells, triggering adaptive immunity.

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14
Q

What are the 5 cardinal signs of inflammation?

A

Calor – heat Rubor – redness Tumour – swelling Dolor – pain Functio laesa – loss of function

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15
Q

What stimulates the complement system?

A

Inflammation, bacteria/viruses/fungi, tissue damage, antibodies.

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16
Q

What are the three complement pathways?

A

Classical, lectin, and alternative.

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17
Q

What are the main outcomes of complement activation?

A

Opsonisation (enhanced phagocytosis) Cell lysis Inflammation

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18
Q

What causes hereditary angioedema?

A

Inherited C1 esterase inhibitor deficiency.

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19
Q

What does lack of C1 esterase inhibitor lead to?

A

Uncontrolled activation of the classical complement pathway → excessive inflammation.

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20
Q

What triggers swelling in HAE?

A

Minor trauma or spontaneous activation.

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21
Q

Dangerous features of HAE?

A

Swelling of lips, cheeks, airway → potential airway obstruction.

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22
Q

Treatment for HAE?

A

C1 esterase inhibitor replacement.

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23
Q

What are antigens?

A

Proteins, peptides, or complex molecules that trigger immune responses.

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24
Q

What is the function of antibodies?

A

Bind antigens via variable region Trigger immune responses via effector region Recruit complement + immune cells Mark antigens for destruction

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25
Where are B cells activated?
Lymph nodes.
26
What happens when an antigen binds a B cell receptor?
B cell is activated Produces specific antibodies Undergoes clonal expansion Produces memory cells → quicker response next time
27
What does cell-mediated immunity target?
Tumour cells Virus-infected cells Non-self cells
28
How do T cells work?
Recognise antigens via T-cell receptor Release cytokines Kill target cells Undergo clonal expansion
29
What is the difference between primary and secondary immune responses?
Primary = slow, low antibody level Secondary = faster and larger response due to memory cells
30
What is immunological memory?
Persistence of antigen-specific lymphocytes in lymph nodes enabling faster responses to repeated exposure.
31
What organism causes tetanus?
Clostridium tetani.
32
How does tetanus toxin work?
Blocks inhibitory neurons → uncontrolled muscle spasms, lockjaw, trismus, respiratory failure.
33
What is tetanus immunoglobulin?
Pre-formed antibodies against tetanus toxin.
34
What are features of passive immunity?
No immune system activation No long-term protection Used when patient is at immediate risk
35
What is a toxoid?
Modified toxin that is antigenic but non-toxic.
36
How does tetanus toxoid work?
Stimulates B cells Produces memory cells Provides long-lasting protection
37
What forms can vaccines take?
Toxins/toxoids Dead/killed bacteria Live attenuated organisms Viral particles DNA/RNA vaccines
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39
What is an antigen?
A molecule (often protein/peptide) that stimulates an immune response.
40
What produces antibodies?
B cells → plasma cells.
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What are the two functional regions of antibodies?
Fab (variable region) → binds antigen Fc (constant region) → binds complement & immune cells
42
What happens when an antibody binds an antigen?
Marks it for phagocytosis Activates complement Signals to immune cells Neutralises toxins/viruses
43
Where do B cells encounter antigens?
Lymph nodes, spleen, circulation.
44
What happens when a B cell receptor binds its antigen?
B cell activation Differentiation into plasma cells Massive antibody secretion Clonal expansion Formation of memory B cells
45
What is clonal expansion?
Rapid multiplication of antigen-specific lymphocytes to amplify immune response.
46
What does cell-mediated immunity target?
Virus-infected cells Tumour cells Foreign tissue Intracellular pathogens
47
How do T cells recognise antigen?
Through the T cell receptor (TCR) presented on MHC molecules.
48
What do cytotoxic T cells do?
Bind antigen Release perforin/granzymes Trigger apoptosis of infected cells
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What do helper T cells do?
Release cytokines Activate B cells Activate macrophages Coordinate immune response
50
What is the primary immune response?
First exposure → slow, weak antibody production.
51
What is the secondary immune response?
Second exposure → rapid, strong, long-lasting due to memory cells.
52
Which cells provide memory in humoral immunity?
Memory B cells.
53
Which cells provide memory in cell-mediated immunity?
Memory T cells.
54
What organism causes tetanus?
Clostridium tetani (found in soil).
55
What does tetanus toxin do?
Blocks inhibitory neurons → uncontrolled muscle contraction → “lockjaw”.
56
What are the dangers of tetanus?
Respiratory failure Severe muscle spasms Trismus Death without treatment
57
What is passive immunity?
Giving pre-made antibodies (e.g., tetanus immunoglobulin).
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Does passive immunity involve the patient’s immune system?
No — no memory formed → no long-term protection.
59
When is passive immunity used?
Immediate protection when patient is exposed to toxin.
60
What is a toxoid?
Modified toxin → antigenic but non-toxic.
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How does a toxoid vaccine work?
Triggers antibody production + memory B cells → long-term protection.
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Types of vaccines?
Live attenuated Inactivated (killed) Subunit Toxoid DNA/RNA vaccines
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Bone/connective tissue autoimmune diseases:
Rheumatoid arthritis SLE
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Endocrine autoimmune diseases:
Type 1 diabetes Addison’s disease Autoimmune thyroiditis (Hashimoto, Graves)
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GI autoimmune diseases:
Coeliac disease Pernicious anaemia
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Nervous system immune diseases:
Multiple sclerosis Myasthenia gravis
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Skin/mucosal diseases:
Pemphigus, pemphigoid
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Salivary/tear gland disease:
Sjögren’s syndrome
69
Heart autoimmune disease:
Rheumatic fever
70
What is MHC?
Major histocompatibility complex — identifies self vs non-self.
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Why is MHC important in transplantation?
Mismatch triggers immune attack → graft rejection.
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What is host-vs-graft disease?
Recipient immune system attacks transplanted organ.
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Why are stem cell transplants used?
Treat blood cancers → replace destroyed bone marrow.
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What is graft-vs-host disease (GVHD)?
Donor immune cells attack recipient tissues.
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Tissues commonly affected by GVHD:
Skin GIT Liver Mouth (lichen planus-like patches)
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Symptoms of chronic GVHD:
* Dry mouth/eyes * Mouth ulcers * Rash Jaundice * SOB * Nausea/vomiting
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Main immunosuppressive drugs:
* Steroids * Methotrexate * Biological agents (e.g., anti-TNF)
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Causes of immunodeficiency:
Chemotherapy Autoimmune disease treatment Transplants Blood cancers Inherited disorders
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What is Organ Rejection?
The recipient’s immune system attacks the transplanted organ because the donor MHC/HLA is different.
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Why Do Organs Get Rejected?
Donor and recipient MHC don’t match. Host’s T cells recognise graft as foreign. Immune response activated → tissue damage.
81
Types of Host-vs-Graft Rejection
Hyperacute: Minutes–hours Pre-existing antibodies attack graft → immediate failure. Acute: Days–weeks Mainly T-cell attack on graft. Treatable with immunosuppression. Chronic: Months–years Slow, long-term damage → fibrosis, narrowing of vessels. Irreversible.
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Humoral (Antibody) Immunity
B cells → antibodies Fights bacteria + viruses In transplants → antibodies can damage graft vessels → antibody-mediated rejection.
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Why Do We Do Stem Cell Transplants?
Used for: Leukaemia (blood cancer) Lymphoma Myeloma Bone marrow failure.
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How Does a Stem Cell Transplant Work?
Chemotherapy/radiotherapy kills patient’s blood cells + marrow. Donor stem cells infused. Donor cells regrow patient’s bone marrow + immune system.
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Main Risk of HSCT
Graft vs Host Disease (GVHD) Because donor T cells see patient’s tissues as foreign and attack them.
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What is GVHD?
Donor immune cells attack host tissues because they recognise host MHC as foreign. Affects: Skin GIT Liver Mouth Eyes and lungs (chronic).
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Acute vs Chronic GVHD
Acute (<100 days): Skin rash Diarrhoea Abdominal pain Liver enzyme rise Oral ulceration Chronic (>100 days): Dry mouth + dry eyes Mouth sores Skin thickening Jaundice Breathlessness Nausea/vomiting Autoimmune-like symptoms.
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Oral Signs of GVHD
Lichen planus-like white patches Ulcers Burning/sensitivity Dry mouth Increased infections (Candida, HSV).
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Why Do We Use Immunosuppressants?
To prevent: Host rejecting graft GVHD Autoimmune flares.
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Main Immunosuppressants
Steroids Reduce inflammation First-line Used for prophylaxis and flares Methotrexate - Stops T/B-cell division Used in GVHD and autoimmune diseases Biologics Target specific immune pathways (e.g., TNF, IL-6, JAK).
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Risks of Immunosuppression
Infections (bacterial, viral, fungal) Poor healing Higher cancer risk Reactivation of latent infections (e.g., TB, herpes).
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What is Immunodeficiency?
Weak or failing immune system. Types: Primary = inherited Secondary = acquired (most common).
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Causes of Secondary Immunodeficiency
Chemotherapy Radiotherapy Steroids Biologics Post-transplant Autoimmune disease treatment Cancer: leukaemia, lymphoma, myeloma.
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Oral Signs of Immunodeficiency
Thrush (Candida) Herpes reactivation Severe periodontal disease Ulcers Slow healing Caries risk ↑ (especially with dry mouth).
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What is Myastenia gravis
Affects neuromuscular junction which can cause weakness as patients are not able to move muscles as they should be able to.
96
Wat is Rheumatic fever
strep infection - antigens look similar to heart- autoimmune reaction to the heart
97
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