5. Immunity& Disease Flashcards by Michele Herbert

Why do you need to know?

Affects all patients
Infections common
Some patients more susceptible to infection
Some medical conditions caused directly by the immune system

How well did you know this?

Not at all

Perfectly

What is Immunity?

Protection or defence against infections…
BACTERIA
VIRUS
FUNGI
Toxins 
Cancer

How well did you know this?

Not at all

Perfectly

Immune System

Distinguishes self from non-self molecules

Activates multiple mechanisms to either eliminate or neutralise threat
2 main pathways
Innate
Adaptive

How well did you know this?

Not at all

Perfectly

Defence against disease

Innate immunity

Adaptive immune reponse

How well did you know this?

Not at all

Perfectly

Innate immunity

Defense mechansims present even before infection or activated in a non-specific way
Skin, mucous membranes
Phagocytic cells (neutrophils, macrophages), inflammation, fever

How well did you know this?

Not at all

Perfectly

Adaptive immune reponse

Cell-mediated immunity

Humoral immunity

How well did you know this?

Not at all

Perfectly

Non-specific defences

Non-specific defenses are designed to prevent infections by viruses and bacteria
These include:
Intact skin
Mucus and Cilia

How well did you know this?

Not at all

Perfectly

Skin

Outer layer of keratin – mechanical barrier
Dead skin cells constantly sloughed off
hard for invading bacteria to colonize
Sweat and oils contain anti-microbial chemicals

How well did you know this?

Not at all

Perfectly

Mucous membranes

Normal flow of mucus washes bacteria and viruses off of mucus membranes
Cilia (hair-like projections on cells) – respiratory tract
Acid – stomach, vagina
Enzymes – saliva, eye

How well did you know this?

Not at all

Perfectly

Chemical barriers

Proteins
Complement - works with other defence mechanisms of the body
Interferons - inhibit the replication of many viruses

How well did you know this?

Not at all

Perfectly

Cellular defences - phagocytosis (1)

Granulocytes
Neutrophils, eosinophils, basophils
Remove dead cells and micro-organisms
Attracted by an inflammatory response of damaged cells

How well did you know this?

Not at all

Perfectly

Cellular defences - phagocytosis (2)

Monocytes
macrophages
In tissues which serve as filters for trapping microbes
Macrophages live longer than granulocytes
Attracted by different stimuli and usually arrive at sites of invasion later than granulocytes
Stimulate specific immune response (‘antigen-presenting’)

How well did you know this?

Not at all

Perfectly

Non-specific responses to infection

-Macrophages release protein signals
interleukin-1 (IL-1) and interleukin-6 (IL-6)
-Fever
Most bacteria grow optimally at temp below body temp
-Pain, swelling, redness
Increasing capillary permeability, promoting blood flow, bringing more phagocytic cells
-Acute-phase proteins released from liver
Bind to bacteria and activate complement proteins

How well did you know this?

Not at all

Perfectly

Specific (adaptive) immunity

Relies on antigens
specific substances found in foreign microbes
Lymphocytes
Can travel swiftly around the body when carried along in the blood or lymph
Approx 2 x 10^12 lymphocytes in human body
Approx 1 % are in the bloodstream
Rest in lymphatic system

How well did you know this?

Not at all

Perfectly

Lymphocytes (1)

Produced in bone marrow
B-cells mature in bone marrow then concentrate in lymph nodes and spleen
T-cells mature in thymus
B and T-cells mature then circulate in the blood and lymph
Circulation ensures they come into contact with pathogens and each other

How well did you know this?

Not at all

Perfectly

Lymphoid tissues

Adenoid
Tonsil
Thymus
Spleen
Appendix
Bone Marrow
Lymph Nodes
Peyers Patch (small intestine)
Lymphoid aggregates (large intestine)
Lymphatics

Lymphocytes (2)

B-cells

T-cells

B-cells

Secrete antibodies
Humoral immunity
Recognise pathogens outside cells

T-cells (1)

Do not recognise free antigen - only recognise antigen presented by major histocompatibility complex – class I (all cells) or class II (APC)
Directly attack invaders (cytotoxic, CD8+, MHC I)
Cell-mediated immunity
Recognise pathogens that have entered cells
Also help B-cells (helper cells, CD4+, MHC II)

T-cells (2)

Cytotoxic

Helper

Cytotoxic

Seek out and destroy any antigens in the system, and destroy microbes “tagged” by antibodies
Some cytotoxic T-cells can recognize and destroy cancer cells
Variable region on T-cell receptor

Helper

Stimulate B-cells

Activate cytotoxic - cells and macrophages to attack infected cells

How do T-cells recognise an invader?

Detect antigen – protein marker on cell surface
(Epitope = fragment of antigen)

If an antigen (“not self”) protein is encountered by a macrophage, it will bring the protein to a helper T-cell for identification.

If the helper T-cell recognizes the protein as “not self,” it will launch an immune response.

Signalling immune response

Helper T-cells (CD4+) stimulated by antigen  cytokines to stimulate B-cell division

HIV destroys helper T-cells so immune response diminished

B-cells (2)

Produce antibodies Glycoproteins Specific, hypervariable region Different subtypes IgG, IgM, IgA, IgE, IgD Opsonisation, bind and block (agglutinate), stimulate complement Bind to antigen on cell or free  plasma cells  more antibody Or become memory cells - remain ready to divide rapidly if an invasion occurs again

Immune System

Vital for survival but can be a double-edged sword Immunodeficiency – prone to infections Overactive immune system- hypersensitivity reactions Failure to recognise self- autoimmune diseases

The Immune System - Deficient

Chemotherapy / Drugs HIV Splenectomy Bone Marrow dysfunction

The Immune System - Hyperactive

Allergy (Hypersensitivity) Auto-immunity Overreaction to Pathogen

Immunodeficiency (1)

``` Drugs Chemotherapy Immunosuppressive Medication Splenectomy Bone Marrow Dysfunction ```

Immunodeficiency (2) | HIV – Human Immunodeficiency Virus

Retrovirus - Infects CD4+ T cells - causes AIDS (Acquired Immunodeficiency Syndrome) Stages of progression : Infection, Latency, AIDS AIDS - decline in CD4+ T-cells, opportunistic infections

Immunodeficiency (3)

Important to know if a patient is immunosupressed More prone to infection Significantly alter the immune response of the patient to infection

Causes of secondary immunodeficiency

``` Malnutrition Burns Uremia Diabetes mellitus Immunotoxic medications Self-medication of recreational drugs and alcohol AIDS ```

Hyperactive (1)

Hypersensitivity Excessive immune reaction against harmless antigen. Type 1 – Type 4 – based on mechanism. Type 1 – Anaphylaxis/Allergy e.g. Asthma, Rhinitis (Hay fever), Peanut allergy. - Sensitization first step.

Hyperactive (2)

Over reaction to pathogen | Systemic Inflammatory Response Syndrome

Hyperactive (3)

Autoimmunity failure of an organism in recognizing its own constituent parts as self leading to an immune response against its own cells and tissues Normally display “self tolerance” Self reactive lymphocytes deleted centrally suppressed in periphery

Autoimmune Diseases

Type 1 Diabetes Mellitus Coeliac Disease Multiple Sclerosis Hashimoto’s Thyroiditis

Manipulation of Immune System

Suppress Immune system Organ transplant - increased susceptibility to infection Cancer – Immunotherapy Vaccination

Vaccination (1)

= Active Immunity Stimulate own immune system to elicit adaptive immune response, prevent future infection. Success depends on Herd Immunity

Vaccination (2)

Live (Attenuated) Vaccines - live, weakened pathogen e.g. MMR Inactivated Vaccines - inactivated, part of pathogen e.g. Hepatitis B Toxoid - bacterial toxin e.g. Diptheria Conjugated - antigen linked to protein carrier e.g. Pneumococcal